https://proteopedia.org/api.php?action=feedcontributions&feedformat=atom&user=Max+Evoy-Mount 2026-09-17T00:42:56Z User contributions MediaWiki 1.43.8 https://proteopedia.org/index.php?title=Shiga_toxin&diff=1314170 2011-11-08T23:57:17Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;StructureSection load=1dm0 size='500' side='right' caption='Stx1', ([[1dm0]])' scene=''&gt;<br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of [http://en.wikipedia.org/wiki/AB5_toxin AB5] toxins (Stx1 and Stx2) which cause [http://en.wikipedia.org/wiki/Dysentery dysentery], [http://en.wikipedia.org/wiki/Hemolytic-uremic_syndrome hemolytic-uremic syndrome], and potentially renal failure in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the [http://en.wikipedia.org/wiki/0157:H7 0157:H7] strain&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; and [http://en.wikipedia.org/wiki/Shigella_dysenteriae shigella dysentarie]. STECs are one of the major foodborne pathogens, affecting both developed and third-world countries. The stx gene is not endogenous to these strains, but is introduced through horizontal gene transfer from environmental prophages of the lambdoid bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; Shiga Toxins are closely related to [[ricin]], which is structurally and mechanistically similar. Shiga toxin acts to inhibit protein synthesis in eukaryotic cells and is the main virulence factor of STEC. <br /> <br /> ==Human Interaction==<br /> 0157:H7 STECs are spread to humans through a fecal-oral mechanism, primarily from ingestion of food contaminated with fecal material. Cattle, goats, and sheep are the primary reservoir of STECs and their close proximity to food sources as well as the use of animal feces for fertilizer makes them the main route of contamination.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; These animals can house STEC's without effect due to a lack of Stx surface receptors.&lt;ref name=Asakura&gt;PMID: 11561972&lt;/ref&gt; Inadequate sanitation and contamination of meat during slaughter can both lead to STEC contaminated food at the market. Once ingested the STEC can survive the high acid environment of the stomach and progress to the gut where they attach firmly to gut mucosa via the [http://en.wikipedia.org/wiki/Intimin intimin adhesin protein].&lt;ref name=Russel&gt;PMID: 11321582&lt;/ref&gt; Secreted Stx then either attacks gut epithelia or passes into the bloodstream where it can damage kidney and brain tissue. <br /> <br /> '''Treatments'''<br /> <br /> Treatment with antibiotics is contraindicated as antibiotic treatment has been demonstrated to increase Stx production up to one hundred fold.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; This results from the link between Stx production (and phage induction) to the [http://en.wikipedia.org/wiki/SOS_response SOS response pathway].&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; In the event of renal failure kidney dialysis may be employed. A number of potential treatments are under development including B subunit inhibitors, polysaccharides that promote macrophage uptake of Stx, blocking of the Gb&lt;sub&gt;3&lt;/sub&gt; membrane receptor, and inhibition of [http://en.wikipedia.org/wiki/Retrograde_transport#Retrograde_transport retrograde transport].&lt;ref name=Nishikiwa&gt;PMID: 21644029&lt;/ref&gt;<br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an AB&lt;sub&gt;5&lt;/sub&gt; hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The <br /> &lt;scene name='Shiga_toxin_1/Subunits/1'&gt;5 subunit B pentamer interacts with the A subunit&lt;/scene&gt; via a &lt;scene name='Shiga_toxin_1/A-b_helixes/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The &lt;scene name='Shiga_toxin_1/Active_site_zoomed_out_a-b/1'&gt;glycosidase active site&lt;/scene&gt; is located on the A subunit, but is blocked by the B subunit until the &lt;scene name='Shiga_toxin_1/Disulphide_bond/1'&gt;disulphide bond between cys242 and cys261&lt;/scene&gt; is cleaved releasing an active A subunit into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 28S ribosomal rRNA of a target cell which leads to inhibition of protein elongation and ultimately cellular apoptosis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to globo series glycolipid globotriaosylceramide (Gb&lt;sub&gt;3&lt;/sub&gt;), a eukaryotic membrane receptor, where it is then endocytosed and proteolytically cleaved into an active A subunit and a B subunit.&lt;ref name=Lenz&gt;PMID: 2170899&lt;/ref&gt; The B subunit is not active in the depurination of of 28S rRNA, but is essential for GB&lt;sub&gt;3&lt;/sub&gt; binding and therefore essential for toxicity. Once in the cytosol the A subunit is free to interact with and inactivate 28S rRNA. On the A subunit &lt;scene name='Shiga_toxin_1/Active_site_zoomed_in/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; This mechanism (B subunit binding to globotriaosylceramide and A subunit depurinating 28S rRNA) is conserved amongst the Stx family as well as the ricin toxin.<br /> &lt;/StructureSection&gt;<br /> <br /> <br /> ==3D structures==<br /> <br /> {{STRUCTURE_2ga4| PDB=2ga4 | SCENE= }}<br /> <br /> [[1dm0]] - Stx1&lt;br /&gt;<br /> [[1r4q]] - Stx2&lt;br /&gt;<br /> [[1r4p]] - Stx2 bound to ligand&lt;br /&gt;<br /> [[2ga4]] - Stx2 with adenine&lt;br /&gt;<br /> <br /> <br /> '''Mutants'''<br /> <br /> [[1c48]] - Shiga-like toxin B subunit&lt;br /&gt;<br /> [[1cqf]] - Shiga-like toxin B subunit bound to trisaccharide&lt;br /&gt;<br /> [[1bos]] - Shiga-like toxin bound to receptor&lt;br /&gt;<br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1314162 2011-11-08T23:35:58Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;StructureSection load=1dm0 size='500' side='right' caption='Stx1', ([[1dm0]])' scene=''&gt;<br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of [http://en.wikipedia.org/wiki/AB5_toxin AB5] toxins (Stx1 and Stx2) which cause [http://en.wikipedia.org/wiki/Dysentery dysentery], [http://en.wikipedia.org/wiki/Hemolytic-uremic_syndrome hemolytic-uremic syndrome], and potentially renal failure in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the [http://en.wikipedia.org/wiki/0157:H7 0157:H7] strain&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; and [http://en.wikipedia.org/wiki/Shigella_dysenteriae shigella dysentarie]. STECs are one of the major foodborne pathogens, affecting both developed and third-world countries. The stx gene is not endogenous to these strains, but is introduced through horizontal gene transfer from environmental prophages of the lambdoid bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; Shiga Toxins are closely related to [[ricin]], which is structurally and mechanistically similar. Shiga toxin acts to inhibit protein synthesis in eukaryotic cells and is the main virulence factor of STEC. <br /> <br /> ==Human Interaction==<br /> 0157:H7 STECs are spread to humans through a fecal-oral mechanism, primarily from ingestion of food contaminated with fecal material. Cattle, goats, and sheep are the primary reservoir of STECs and their close proximity to food sources as well as the use of animal feces for fertilizer makes them the main route of contamination.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; These animals can house STEC's without effect due to a lack of Stx surface receptors.&lt;ref name=Asakura&gt;PMID: 11561972&lt;/ref&gt; Inadequate sanitation and contamination of meat during slaughter can both lead to STEC contaminated food at the market. Once ingested the STEC can survive the high acid environment of the stomach and progress to the gut where they attach firmly to gut mucosa via the [http://en.wikipedia.org/wiki/Intimin intimin adhesin protein].&lt;ref name=Russel&gt;PMID: 11321582&lt;/ref&gt; Secreted Stx then either attacks gut epithelia or passes into the bloodstream where it can damage kidney and brain tissue. <br /> <br /> '''Treatments'''<br /> <br /> Treatment with antibiotics is contraindicated as antibiotic treatment has been demonstrated to increase Stx production up to one hundred fold.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; This results from the link between Stx production (and phage induction) to the [http://en.wikipedia.org/wiki/SOS_response SOS response pathway].&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; In the event of renal failure kidney dialysis may be employed. A number of potential treatments are under development including B subunit inhibitors, polysaccharides that promote macrophage uptake of Stx, blocking of the Gb&lt;sub&gt;3&lt;/sub&gt; membrane receptor, and inhibition of [http://en.wikipedia.org/wiki/Retrograde_transport#Retrograde_transport retrograde transport].&lt;ref name=Nishikiwa&gt;PMID: 21644029&lt;/ref&gt;<br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an AB&lt;sub&gt;5&lt;/sub&gt; hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The <br /> &lt;scene name='Shiga_toxin_1/Subunits/1'&gt;5 subunit B pentamer interacts with the A subunit&lt;/scene&gt; via a &lt;scene name='Shiga_toxin_1/A-b_helixes/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The &lt;scene name='Shiga_toxin_1/Active_site_zoomed_out_a-b/1'&gt;glycosidase active site&lt;/scene&gt; is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 28S ribosomal rRNA of a target cell which leads to inhibition of protein elongation and ultimately cellular apoptosis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to globo series glycolipid globotriaosylceramide (Gb&lt;sub&gt;3&lt;/sub&gt;), a eukaryotic membrane receptor, where it is then endocytosed and proteolytically cleaved into an active A subunit and a B subunit.&lt;ref name=Lenz&gt;PMID: 2170899&lt;/ref&gt; The B subunit is not active in the depurination of of 28S rRNA, but is essential for GB&lt;sub&gt;3&lt;/sub&gt; binding and therefore essential for toxicity. Once in the cytosol the A subunit is free to interact with and inactivate 28S rRNA. On the A subunit &lt;scene name='Shiga_toxin_1/Active_site_zoomed_in/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; This mechanism (B subunit binding to globotriaosylceramide and A subunit depurinating 28S rRNA) is conserved amongst the Stx family as well as the ricin toxin.<br /> &lt;/StructureSection&gt;<br /> <br /> <br /> ==3D structures==<br /> <br /> {{STRUCTURE_2ga4| PDB=2ga4 | SCENE= }}<br /> <br /> [[1dm0]] - Stx1&lt;br /&gt;<br /> [[1r4q]] - Stx2&lt;br /&gt;<br /> [[1r4p]] - Stx2 bound to ligand&lt;br /&gt;<br /> [[2ga4]] - Stx2 with adenine&lt;br /&gt;<br /> <br /> <br /> '''Mutants'''<br /> <br /> [[1c48]] - Shiga-like toxin B subunit&lt;br /&gt;<br /> [[1cqf]] - Shiga-like toxin B subunit bound to trisaccharide&lt;br /&gt;<br /> [[1bos]] - Shiga-like toxin bound to receptor&lt;br /&gt;<br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1314157 2011-11-08T23:22:12Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;StructureSection load=1dm0 size='500' side='right' caption='Stx1', ([[1dm0]])' scene=''&gt;<br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of [http://en.wikipedia.org/wiki/AB5_toxin AB5] toxins (Stx1 and Stx2) which cause [http://en.wikipedia.org/wiki/Dysentery dysentery], [http://en.wikipedia.org/wiki/Hemolytic-uremic_syndrome hemolytic-uremic syndrome], and potentially renal failure in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the [http://en.wikipedia.org/wiki/0157:H7 0157:H7] strain&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; and [http://en.wikipedia.org/wiki/Shigella_dysenteriae shigella dysentarie]. STECs are one of the major foodborne pathogens, affecting both developed and third-world countries. The stx gene is not endogenous to these strains, but is introduced through horizontal gene transfer from environmental prophages of the lambdoid bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; Shiga Toxins are closely related to [[ricin]], which is structurally and mechanistically similar. Shiga toxin acts to inhibit protein synthesis in eukaryotic cells and is the main virulence factor of STEC. <br /> <br /> ==Human Interaction==<br /> 0157:H7 STECs are spread to humans through a fecal-oral mechanism, primarily from ingestion of food contaminated with fecal material. Cattle, goats, and sheep are the primary reservoir of STECs and their close proximity to food sources as well as the use of animal feces for fertilizer makes them the main route of contamination.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; Inadequate sanitation and contamination of meat during slaughter can both lead to STEC contaminated food at the market. Once ingested the STEC can survive the high acid environment of the stomach and progress to the gut where they attach firmly to gut mucosa via the [http://en.wikipedia.org/wiki/Intimin intimin adhesin protein].&lt;ref name=Russel&gt;PMID: 11321582&lt;/ref&gt; Secreted Stx then either attacks gut epithelia or passes into the bloodstream where it can damage kidney and brain tissue. <br /> <br /> '''Treatments'''<br /> <br /> Treatment with antibiotics is contraindicated as antibiotic treatment has been demonstrated to increase Stx production up to one hundred fold.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; This results from the link between Stx production (and phage induction) to the [http://en.wikipedia.org/wiki/SOS_response SOS response pathway].&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; In the event of renal failure kidney dialysis may be employed. A number of potential treatments are under development including B subunit inhibitors, polysaccharides that promote macrophage uptake of Stx, blocking of the Gb&lt;sub&gt;3&lt;/sub&gt; membrane receptor, and inhibition of [http://en.wikipedia.org/wiki/Retrograde_transport#Retrograde_transport retrograde transport].&lt;ref name=Nishikiwa&gt;PMID: 21644029&lt;/ref&gt;<br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an AB&lt;sub&gt;5&lt;/sub&gt; hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The <br /> &lt;scene name='Shiga_toxin_1/Subunits/1'&gt;5 subunit B pentamer interacts with the A subunit&lt;/scene&gt; via a &lt;scene name='Shiga_toxin_1/A-b_helixes/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The &lt;scene name='Shiga_toxin_1/Active_site_zoomed_out_a-b/1'&gt;glycosidase active site&lt;/scene&gt; is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to globo series glycolipid globotriaosylceramide (Gb&lt;sub&gt;3&lt;/sub&gt;), a eukaryotic membrane receptor, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit.&lt;ref name=Lenz&gt;PMID: 2170899&lt;/ref&gt; Once the A subunit is transported to the cytosol it acts by depurinating the 28S ribosomal RNA which leads to inhibition of protein elongation and ultimately cellular apoptosis. On the A subunit &lt;scene name='Shiga_toxin_1/Active_site_zoomed_in/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> &lt;/StructureSection&gt;<br /> <br /> <br /> ==3D structures==<br /> <br /> {{STRUCTURE_2ga4| PDB=2ga4 | SCENE= }}<br /> <br /> [[1dm0]] - Stx1&lt;br /&gt;<br /> [[1r4q]] - Stx2&lt;br /&gt;<br /> [[1r4p]] - Stx2 bound to ligand&lt;br /&gt;<br /> [[2ga4]] - Stx2 with adenine&lt;br /&gt;<br /> <br /> <br /> '''Mutants'''<br /> <br /> [[1c48]] - Shiga-like toxin B subunit&lt;br /&gt;<br /> [[1cqf]] - Shiga-like toxin B subunit bound to trisaccharide&lt;br /&gt;<br /> [[1bos]] - Shiga-like toxin bound to receptor&lt;br /&gt;<br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1314153 2011-11-08T23:06:39Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;StructureSection load=1dm0 size='500' side='right' caption='Stx1', ([[1dm0]])' scene=''&gt;<br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of [http://en.wikipedia.org/wiki/AB5_toxin AB5] toxins (Stx1 and Stx2) which cause dysentery, hemolytic-uremic syndrome, and potentially renal failure in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; and shigella dysentarie. STECs are one of the major foodborne pathogens, affecting both developed and third-world countries. The stx gene is not endogenous to these strains, but is introduced through horizontal gene transfer from environmental prophages of the lambdoid bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; Shiga Toxins are closely related to [[ricin]], which is structurally and mechanistically similar. Shiga toxin acts to inhibit protein synthesis in eukaryotic cells and is the main virulence factor of STEC. <br /> <br /> ==Human Interaction==<br /> 0157:H7 STECs are spread to humans through a fecal-oral mechanism, primarily from ingestion of food contaminated with fecal material. Cattle, goats, and sheep are the primary reservoir of STECs and their close proximity to food sources as well as the use of animal feces for fertilizer makes them the main route of contamination.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; Inadequate sanitation and contamination of meat during slaughter can both lead to STEC contaminated food at the market. Once ingested the STEC can survive the high acid environment of the stomach and progress to the gut where they attach firmly to gut mucosa via the [http://en.wikipedia.org/wiki/Intimin intimin adhesin protein].&lt;ref name=Russel&gt;PMID: 11321582&lt;/ref&gt; Secreted Stx then either attacks gut epithelia or passes into the bloodstream where it can damage kidney and brain tissue. <br /> <br /> '''Treatments'''<br /> <br /> Treatment with antibiotics is contraindicated as antibiotic treatment has been demonstrated to increase Stx production up to one hundred fold.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; This results from the link between Stx production (and phage induction) to the [http://en.wikipedia.org/wiki/SOS_response SOS response pathway].&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; In the event of renal failure kidney dialysis may be employed. A number of potential treatments are under development including B subunit inhibitors, polysaccharides that promote macrophage uptake of Stx, blocking of the Gb&lt;sub&gt;3&lt;/sub&gt; membrane receptor, and inhibition of [http://en.wikipedia.org/wiki/Retrograde_transport#Retrograde_transport retrograde transport].&lt;ref name=Nishikiwa&gt;PMID: 21644029&lt;/ref&gt;<br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an AB&lt;sub&gt;5&lt;/sub&gt; hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The <br /> &lt;scene name='Shiga_toxin_1/Subunits/1'&gt;5 subunit B pentamer interacts with the A subunit&lt;/scene&gt; via a &lt;scene name='Shiga_toxin_1/A-b_helixes/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The &lt;scene name='Shiga_toxin_1/Active_site_zoomed_out_a-b/1'&gt;glycosidase active site&lt;/scene&gt; is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to globo series glycolipid globotriaosylceramide (Gb&lt;sub&gt;3&lt;/sub&gt;), a eukaryotic membrane receptor, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit.&lt;ref name=Lenz&gt;PMID: 2170899&lt;/ref&gt; Once the A subunit is transported to the cytosol it acts by depurinating the 28S ribosomal RNA which leads to inhibition of protein elongation and ultimately cellular apoptosis. On the A subunit &lt;scene name='Shiga_toxin_1/Active_site_zoomed_in/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> &lt;/StructureSection&gt;<br /> <br /> <br /> ==3D structures==<br /> <br /> {{STRUCTURE_2ga4| PDB=2ga4 | SCENE= }}<br /> <br /> [[1dm0]] - Stx1&lt;br /&gt;<br /> [[1r4q]] - Stx2&lt;br /&gt;<br /> [[1r4p]] - Stx2 bound to ligand&lt;br /&gt;<br /> [[2ga4]] - Stx2 with adenine&lt;br /&gt;<br /> <br /> <br /> '''Mutants'''<br /> <br /> [[1c48]] - Shiga-like toxin B subunit&lt;br /&gt;<br /> [[1cqf]] - Shiga-like toxin B subunit bound to trisaccharide&lt;br /&gt;<br /> [[1bos]] - Shiga-like toxin bound to receptor&lt;br /&gt;<br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=User:Max_Evoy-Mount/Sandbox1&diff=1314146 2011-11-08T23:00:38Z

<p>Max Evoy-Mount: New page: [http://www.example.com link title]</p> <hr /> <div>[http://www.example.com link title]</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1313980 2011-11-07T17:43:34Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;StructureSection load=1dm0 size='500' side='right' caption='Stx1', ([[1dm0]])' scene=''&gt;<br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of [http://en.wikipedia.org/wiki/AB5_toxin AB5] toxins (Stx1 and Stx2) which cause dysentery, hemolytic-uremic syndrome, and potentially renal failure in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; and shigella dysentarie. STECs are one of the major foodborne pathogens, affecting both developed and third-world countries. The stx gene is not endogenous to these strains, but is introduced through horizontal gene transfer from environmental prophages of the lambdoid bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; Shiga Toxins are closely related to [[ricin]], which is structurally and mechanistically similar. Shiga toxin acts to inhibit protein synthesis in eukaryotic cells and is the main virulence factor of STEC. <br /> <br /> ==Human Interaction==<br /> 0157:H7 STECs are spread to humans through a fecal-oral mechanism, primarily from ingestion of food contaminated with fecal material. Cattle, goats, and sheep are the primary reservoir of STECs and their close proximity to food sources as well as the use of animal feces for fertilizer makes them the main route of contamination.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; Inadequate sanitation and contamination of meat during slaughter can both lead to STEC contaminated food at the market. Once ingested the STEC can survive the high acid environment of the stomach and progress to the gut where they attach firmly to gut mucosa via the [http://en.wikipedia.org/wiki/Intimin intimin adhesin protein].&lt;ref name=Russel&gt;PMID: 11321582&lt;/ref&gt; Secreted Stx then either attacks gut epithelia or passes into the bloodstream where it can damage kidney and brain tissue. <br /> <br /> '''Treatments'''<br /> <br /> Treatment with antibiotics is contraindicated as antibiotic treatment has been demonstrated to increase Stx production up to one hundred fold.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; This results from the link between Stx production (and phage induction) to the [http://en.wikipedia.org/wiki/SOS_response SOS response pathway].&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; In the event of renal failure kidney dialysis may be employed. A number of potential treatments are under development including B subunit inhibitors, polysaccharides that promote macrophage uptake of Stx, blocking of the Gb&lt;sub&gt;3&lt;/sub&gt; membrane receptor, and inhibition of [http://en.wikipedia.org/wiki/Retrograde_transport#Retrograde_transport retrograde transport].&lt;ref name=Nishikiwa&gt;PMID: 21644029&lt;/ref&gt;<br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an AB5 hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The <br /> &lt;scene name='Shiga_toxin_1/Subunits/1'&gt;5 subunit B pentamer interacts with the A subunit&lt;/scene&gt; via a &lt;scene name='Shiga_toxin_1/A-b_helixes/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The &lt;scene name='Shiga_toxin_1/Active_site_zoomed_out_a-b/1'&gt;glycosidase active site&lt;/scene&gt; is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to globo series glycolipid globotriaosylceramide (Gb&lt;sub&gt;3&lt;/sub&gt;), a eukaryotic membrane receptor, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit.&lt;ref name=Lenz&gt;PMID: 2170899&lt;/ref&gt; Once the A subunit is transported to the cytosol it acts by depurinating the 28S ribosomal RNA which leads to inhibition of protein elongation and ultimately cellular apoptosis. On the A subunit &lt;scene name='Shiga_toxin_1/Active_site_zoomed_in/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> &lt;/StructureSection&gt;<br /> <br /> <br /> ==3D structures==<br /> <br /> {{STRUCTURE_2ga4| PDB=2ga4 | SCENE= }}<br /> <br /> [[1dm0]] - Stx1&lt;br /&gt;<br /> [[1r4q]] - Stx2&lt;br /&gt;<br /> [[1r4p]] - Stx2 bound to ligand&lt;br /&gt;<br /> [[2ga4]] - Stx2 with adenine&lt;br /&gt;<br /> <br /> <br /> '''Mutants'''<br /> <br /> [[1c48]] - Shiga-like toxin B subunit&lt;br /&gt;<br /> [[1cqf]] - Shiga-like toxin B subunit bound to trisaccharide&lt;br /&gt;<br /> [[1bos]] - Shiga-like toxin bound to receptor&lt;br /&gt;<br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1313979 2011-11-07T17:42:53Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;StructureSection load=1dm0 size='500' side='right' caption='Stx1', ([[1dm0]])' scene=''&gt;<br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of [http://en.wikipedia.org/wiki/AB5_toxin AB5] toxins (Stx1 and Stx2) which cause dysentery, hemolytic-uremic syndrome, and potentially renal failure in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; and shigella dysentarie. STECs are one of the major foodborne pathogens, affecting both developed and third-world countries. The stx gene is not endogenous to these strains, but is introduced through horizontal gene transfer from environmental prophages of the lambdoid bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; Shiga Toxins are closely related to [[ricin]], which is structurally and mechanistically similar. Shiga toxin acts to inhibit protein synthesis in eukaryotic cells and is the main virulence factor of STEC. <br /> <br /> ==Human Interaction==<br /> 0157:H7 STECs are spread to humans through a fecal-oral mechanism, primarily from ingestion of food contaminated with fecal material. Cattle, goats, and sheep are the primary reservoir of STECs and their close proximity to food sources as well as the use of animal feces for fertilizer makes them the main route of contamination.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; Inadequate sanitation and contamination of meat during slaughter can both lead to STEC contaminated food at the market. Once ingested the STEC can survive the high acid environment of the stomach and progress to the gut where they attach firmly to gut mucosa via the [http://en.wikipedia.org/wiki/Intimin intimin adhesin protein].&lt;ref name=Russel&gt;PMID: 11321582&lt;/ref&gt; Secreted Stx then either attacks gut epithelia or passes into the bloodstream where it can damage kidney and brain tissue. <br /> <br /> '''Treatments'''<br /> <br /> Treatment with antibiotics is contraindicated as antibiotic treatment has been demonstrated to increase Stx production up to one hundred fold.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; This results from the link between Stx production (and phage induction) to the [http://en.wikipedia.org/wiki/SOS_response SOS response pathway].&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; In the event of renal failure kidney dialysis may be employed. A number of potential treatments are under development including B subunit inhibitors, polysaccharides that promote macrophage uptake of Stx, blocking of the GB3 membrane receptor, and inhibition of [http://en.wikipedia.org/wiki/Retrograde_transport#Retrograde_transport retrograde transport].&lt;ref name=Nishikiwa&gt;PMID: 21644029&lt;/ref&gt;<br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an AB5 hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The <br /> &lt;scene name='Shiga_toxin_1/Subunits/1'&gt;5 subunit B pentamer interacts with the A subunit&lt;/scene&gt; via a &lt;scene name='Shiga_toxin_1/A-b_helixes/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The &lt;scene name='Shiga_toxin_1/Active_site_zoomed_out_a-b/1'&gt;glycosidase active site&lt;/scene&gt; is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to globo series glycolipid globotriaosylceramide (Gb&lt;sub&gt;3&lt;/sub&gt;), a eukaryotic membrane receptor, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit.&lt;ref name=Lenz&gt;PMID: 2170899&lt;/ref&gt; Once the A subunit is transported to the cytosol it acts by depurinating the 28S ribosomal RNA which leads to inhibition of protein elongation and ultimately cellular apoptosis. On the A subunit &lt;scene name='Shiga_toxin_1/Active_site_zoomed_in/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> &lt;/StructureSection&gt;<br /> <br /> <br /> ==3D structures==<br /> <br /> {{STRUCTURE_2ga4| PDB=2ga4 | SCENE= }}<br /> <br /> [[1dm0]] - Stx1&lt;br /&gt;<br /> [[1r4q]] - Stx2&lt;br /&gt;<br /> [[1r4p]] - Stx2 bound to ligand&lt;br /&gt;<br /> [[2ga4]] - Stx2 with adenine&lt;br /&gt;<br /> <br /> <br /> '''Mutants'''<br /> <br /> [[1c48]] - Shiga-like toxin B subunit&lt;br /&gt;<br /> [[1cqf]] - Shiga-like toxin B subunit bound to trisaccharide&lt;br /&gt;<br /> [[1bos]] - Shiga-like toxin bound to receptor&lt;br /&gt;<br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1313978 2011-11-07T17:40:44Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;StructureSection load=1dm0 size='500' side='right' caption='Stx1', ([[1dm0]])' scene=''&gt;<br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of [http://en.wikipedia.org/wiki/AB5_toxin AB5] toxins (Stx1 and Stx2) which cause dysentery, hemolytic-uremic syndrome, and potentially renal failure in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; and shigella dysentarie. STECs are one of the major foodborne pathogens, affecting both developed and third-world countries. The stx gene is not endogenous to these strains, but is introduced through horizontal gene transfer from environmental prophages of the lambdoid bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; Shiga Toxins are closely related to [[ricin]], which is structurally and mechanistically similar. Shiga toxin acts to inhibit protein synthesis in eukaryotic cells and is the main virulence factor of STEC. <br /> <br /> ==Human Interaction==<br /> 0157:H7 STECs are spread to humans through a fecal-oral mechanism, primarily from ingestion of food contaminated with fecal material. Cattle, goats, and sheep are the primary reservoir of STECs and their close proximity to food sources as well as the use of animal feces for fertilizer makes them the main route of contamination.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; Inadequate sanitation and contamination of meat during slaughter can both lead to STEC contaminated food at the market. Once ingested the STEC can survive the high acid environment of the stomach and progress to the gut where they attach firmly to gut mucosa via the [http://en.wikipedia.org/wiki/Intimin intimin adhesin protein].&lt;ref name=Russel&gt;PMID: 11321582&lt;/ref&gt; Secreted Stx then either attacks gut epithelia or passes into the bloodstream where it can damage kidney and brain tissue. <br /> <br /> '''Treatments'''<br /> <br /> Treatment with antibiotics is contraindicated as antibiotic treatment has been demonstrated to increase Stx production up to one hundred fold.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; This results from the link between Stx production (and phage induction) to the [http://en.wikipedia.org/wiki/SOS_response SOS response pathway].&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; In the event of renal failure kidney dialysis may be employed. A number of potential treatments are under development including B subunit inhibitors, polysaccharides that promote macrophage uptake of Stx, blocking of the GB3 membrane receptor, and inhibition of [http://en.wikipedia.org/wiki/Retrograde_transport#Retrograde_transport retrograde transport].&lt;ref name=Nishikiwa&gt;PMID: 21644029&lt;/ref&gt;<br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an AB5 hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The <br /> &lt;scene name='Shiga_toxin_1/Subunits/1'&gt;5 subunit B pentamer interacts with the A subunit&lt;/scene&gt; via a &lt;scene name='Shiga_toxin_1/A-b_helixes/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The &lt;scene name='Shiga_toxin_1/Active_site_zoomed_out_a-b/1'&gt;glycosidase active site&lt;/scene&gt; is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to globo series glycolipid globotriaosylceramide (Gb3), a eukaryotic membrane receptor, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit.&lt;ref name=Lenz&gt;PMID: 2170899&lt;/ref&gt; Once the A subunit is transported to the cytosol it acts by depurinating the 28S ribosomal RNA which leads to inhibition of protein elongation and ultimately cellular apoptosis. On the A subunit &lt;scene name='Shiga_toxin_1/Active_site_zoomed_in/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> &lt;/StructureSection&gt;<br /> <br /> <br /> ==3D structures==<br /> <br /> {{STRUCTURE_2ga4| PDB=2ga4 | SCENE= }}<br /> <br /> [[1dm0]] - Stx1&lt;br /&gt;<br /> [[1r4q]] - Stx2&lt;br /&gt;<br /> [[1r4p]] - Stx2 bound to ligand&lt;br /&gt;<br /> [[2ga4]] - Stx2 with adenine&lt;br /&gt;<br /> <br /> <br /> '''Mutants'''<br /> <br /> [[1c48]] - Shiga-like toxin B subunit&lt;br /&gt;<br /> [[1cqf]] - Shiga-like toxin B subunit bound to trisaccharide&lt;br /&gt;<br /> [[1bos]] - Shiga-like toxin bound to receptor&lt;br /&gt;<br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=User:Max_Evoy-Mount&diff=1313977 2011-11-07T17:20:40Z

<p>Max Evoy-Mount: </p> <hr /> <div>*[[User:Max Evoy-Mount/Sandbox1]]<br /> <br /> Senior in Microbiology at UCSB<br /> <br /> The page for Shiga Toxin 1 was constructed for Dr. Duane Sears' course MCDB 108AL (protein lab) at University California Santa Barbara</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1313963 2011-11-07T04:58:02Z

<p>Max Evoy-Mount: </p> <hr /> <div>==Introduction==<br /> '''Shiga Toxins''' are a family of [http://en.wikipedia.org/wiki/AB5_toxin AB5] toxins (Stx1 and Stx2) which cause dysentery, hemolytic-uremic syndrome, and potentially renal failure in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; and shigella dysentarie. STECs are one of the major foodborne pathogens, affecting both developed and third-world countries. The stx gene is not endogenous to these strains, but is introduced through horizontal gene transfer from environmental prophages of the lambdoid bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; Shiga Toxins are closely related to [[ricin]], which is structurally and mechanistically similar. Shiga toxin acts to inhibit protein synthesis in eukaryotic cells and is the main virulence factor of STEC. <br /> <br /> {{STRUCTURE_2ga4| PDB=2ga4 | SCENE= }}<br /> <br /> {{STRUCTURE_1dm0| PDB=1dm0 | SCENE= }}<br /> <br /> ==Human Interaction==<br /> 0157:H7 STECs are spread to humans through a fecal-oral mechanism, primarily from ingestion of food contaminated with fecal material. Cattle, goats, and sheep are the primary reservoir of STECs and their close proximity to food sources as well as the use of animal feces for fertilizer makes them the main route of contamination.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; Inadequate sanitation and contamination of meat during slaughter can both lead to STEC contaminated food at the market. Once ingested the STEC can survive the high acid environment of the stomach and progress to the gut where they attach firmly to gut mucosa via the [http://en.wikipedia.org/wiki/Intimin intimin adhesin protein].&lt;ref name=Russel&gt;PMID: 11321582&lt;/ref&gt; Secreted Stx then either attacks gut epithelia or passes into the bloodstream where it can damage kidney and brain tissue. <br /> <br /> '''Treatments'''<br /> <br /> Treatment with antibiotics is contraindicated as antibiotic treatment has been demonstrated to increase Stx production up to one hundred fold.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; This results from the link between Stx production (and phage induction) to the [http://en.wikipedia.org/wiki/SOS_response SOS response pathway].&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; In the event of renal failure kidney dialysis may be employed. A number of potential treatments are under development including B subunit inhibitors, polysaccharides that promote macrophage uptake of Stx, blocking of the GB3 membrane receptor, and inhibition of [http://en.wikipedia.org/wiki/Retrograde_transport#Retrograde_transport retrograde transport].&lt;ref name=Nishikiwa&gt;PMID: 21644029&lt;/ref&gt;<br /> <br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an AB5 hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The <br /> &lt;scene name='Shiga_toxin_1/Subunits/1'&gt;5 subunit B pentamer interacts with the A subunit&lt;/scene&gt; via a &lt;scene name='Shiga_toxin_1/A-b_helixes/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The &lt;scene name='Shiga_toxin_1/Active_site_zoomed_out_a-b/1'&gt;glycosidase active site&lt;/scene&gt; is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to globo series glycolipid globotriaosylceramide (Gb3), a eukaryotic membrane receptor, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit.&lt;ref name=Lenz&gt;PMID: 2170899&lt;/ref&gt; Once the A subunit is transported to the cytosol it acts by depurinating the 28S ribosomal RNA which leads to inhibition of protein elongation and ultimately cellular apoptosis. On the A subunit &lt;scene name='Shiga_toxin_1/Active_site_zoomed_in/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> <br /> <br /> ==3D structures==<br /> <br /> [[1dm0]] - Stx1&lt;br /&gt;<br /> [[1r4q]] - Stx2&lt;br /&gt;<br /> [[1r4p]] - Stx2 bound to ligand&lt;br /&gt;<br /> [[2ga4]] - Stx2 with adenine&lt;br /&gt;<br /> <br /> '''Mutants'''<br /> <br /> [[1c48]] - Shiga-like toxin B subunit&lt;br /&gt;<br /> [[1cqf]] - Shiga-like toxin B subunit bound to trisaccharide&lt;br /&gt;<br /> [[1bos]] - Shiga-like toxin bound to receptor&lt;br /&gt;<br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1313904 2011-11-07T03:23:50Z

<p>Max Evoy-Mount: </p> <hr /> <div>==Introduction==<br /> '''Shiga Toxins''' are a family of [http://en.wikipedia.org/wiki/AB5_toxin AB5] toxins (Stx1 and Stx2) which cause dysentery, hemolytic-uremic syndrome, and potentially renal failure in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; and shigella dysentarie. STECs are one of the major foodborne pathogens, affecting both developed and third-world countries. The stx gene is not endogenous to these strains, but is introduced through horizontal gene transfer from environmental prophages of the lambdoid bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; Shiga Toxins are closely related to [[ricin]], which is structurally and mechanistically similar. Shiga toxin acts to inhibit protein synthesis in eukaryotic cells and is the main virulence factor of STEC. <br /> <br /> {{STRUCTURE_2ga4| PDB=2ga4 | SCENE= }}<br /> <br /> {{STRUCTURE_1dm0| PDB=1dm0 | SCENE= }}<br /> <br /> ==Human Interaction==<br /> 0157:H7 STECs are spread to humans through a fecal-oral mechanism, primarily from ingestion of food contaminated with fecal material. Cattle, goats, and sheep are the primary reservoir of STECs and their close proximity to food sources as well as the use of animal feces for fertilizer makes them the main route of contamination.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; Inadequate sanitation and contamination of meat during slaughter can both lead to STEC contaminated food at the market. Once ingested the STEC can survive the high acid environment of the stomach and progress to the gut where they attach firmly to gut mucosa via the [http://en.wikipedia.org/wiki/Intimin intimin adhesin protein].&lt;ref name=Russel&gt;PMID: 11321582&lt;/ref&gt; Secreted Stx then either attacks gut epithelia or passes into the bloodstream where it can damage kidney and brain tissue. <br /> <br /> '''Treatments'''<br /> <br /> Treatment with antibiotics is contraindicated as antibiotic treatment has been demonstrated to increase Stx production up to one hundred fold.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; This results from the link between Stx production (and phage induction) to the [http://en.wikipedia.org/wiki/SOS_response SOS response pathway].&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; In the event of renal failure kidney dialysis may be employed. A number of potential treatments are under development including B subunit inhibitors, polysaccharides that promote macrophage uptake of Stx, blocking of the GB3 membrane receptor, and inhibition of [http://en.wikipedia.org/wiki/Retrograde_transport#Retrograde_transport retrograde transport].&lt;ref name=Nishikiwa&gt;PMID: 21644029&lt;/ref&gt;<br /> <br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an AB5 hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The <br /> &lt;scene name='Shiga_toxin_1/Subunits/1'&gt;5 subunit B pentamer interacts with the A subunit&lt;/scene&gt; via a <br /> &lt;scene name='Shiga_toxin/A-b_interaction/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The &lt;scene name='Shiga_toxin_1/Active_site_zoomed_out_a-b/1'&gt;glycosidase active site&lt;/scene&gt; is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to globo series glycolipid globotriaosylceramide (Gb3), a eukaryotic membrane receptor, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit.&lt;ref name=Lenz&gt;PMID: 2170899&lt;/ref&gt; Once the A subunit is transported to the cytosol it acts by depurinating the 28S ribosomal RNA which leads to inhibition of protein elongation and ultimately cellular apoptosis. On the A subunit &lt;scene name='Shiga_toxin_1/Active_site_zoomed_in/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> <br /> <br /> ==3D structures==<br /> <br /> [[1dm0]] - Stx1&lt;br /&gt;<br /> [[1r4q]] - Stx2&lt;br /&gt;<br /> [[1r4p]] - Stx2 bound to ligand&lt;br /&gt;<br /> [[2ga4]] - Stx2 with adenine&lt;br /&gt;<br /> <br /> '''Mutants'''<br /> <br /> [[1c48]] - Shiga-like toxin B subunit&lt;br /&gt;<br /> [[1cqf]] - Shiga-like toxin B subunit bound to trisaccharide&lt;br /&gt;<br /> [[1bos]] - Shiga-like toxin bound to receptor&lt;br /&gt;<br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1313900 2011-11-07T02:56:38Z

<p>Max Evoy-Mount: </p> <hr /> <div>==Introduction==<br /> '''Shiga Toxins''' are a family of [http://en.wikipedia.org/wiki/AB5_toxin AB5] toxins (Stx1 and Stx2) which cause dysentery, hemolytic-uremic syndrome, and potentially renal failure in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; and shigella dysentarie. STECs are one of the major foodborne pathogens, affecting both developed and third-world countries. The stx gene is not endogenous to these strains, but is introduced through horizontal gene transfer from environmental prophages of the lambdoid bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; Shiga Toxins are closely related to [[ricin]], which is structurally and mechanistically similar. Shiga toxin acts to inhibit protein synthesis in eukaryotic cells and is the main virulence factor of STEC. <br /> <br /> {{STRUCTURE_2ga4| PDB=2ga4 | SCENE= }}<br /> <br /> {{STRUCTURE_1dm0| PDB=1dm0 | SCENE= }}<br /> <br /> ==Human Interaction==<br /> 0157:H7 STECs are spread to humans through a fecal-oral mechanism, primarily from ingestion of food contaminated with fecal material. Cattle, goats, and sheep are the primary reservoir of STECs and their close proximity to food sources as well as the use of animal feces for fertilizer makes them the main route of contamination.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; Inadequate sanitation and contamination of meat during slaughter can both lead to STEC contaminated food at the market. Once ingested the STEC can survive the high acid environment of the stomach and progress to the gut where they attach firmly to gut mucosa via the [http://en.wikipedia.org/wiki/Intimin intimin adhesin protein].&lt;ref name=Russel&gt;PMID: 11321582&lt;/ref&gt; Secreted Stx then either attacks gut epithelia or passes into the bloodstream where it can damage kidney and brain tissue. <br /> <br /> '''Treatments'''<br /> <br /> Treatment with antibiotics is contraindicated as antibiotic treatment has been demonstrated to increase Stx production up to one hundred fold.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; This results from the link between Stx production (and phage induction) to the [http://en.wikipedia.org/wiki/SOS_response SOS response pathway].&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; In the event of renal failure kidney dialysis may be employed. A number of potential treatments are under development including B subunit inhibitors, polysaccharides that promote macrophage uptake of Stx, blocking of the GB3 membrane receptor, and inhibition of [http://en.wikipedia.org/wiki/Retrograde_transport#Retrograde_transport retrograde transport].&lt;ref name=Nishikiwa&gt;PMID: 21644029&lt;/ref&gt;<br /> <br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an AB5 hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The &lt;scene name='Shiga_toxin/B_subunits/1'&gt;5 subunit B pentamer&lt;/scene&gt; interacts with the &lt;scene name='Shiga_toxin/A_subunits/1'&gt;two separate A subunits&lt;/scene&gt; via a <br /> &lt;scene name='Shiga_toxin/A-b_interaction/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The &lt;scene name='Shiga_toxin_1/Active_site_zoomed_out_a-b/1'&gt;glycosidase active site&lt;/scene&gt; is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to globo series glycolipid globotriaosylceramide (Gb3), a eukaryotic membrane receptor, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit.&lt;ref name=Lenz&gt;PMID: 2170899&lt;/ref&gt; Once the A subunit is transported to the cytosol it acts by depurinating the 28S ribosomal RNA which leads to inhibition of protein elongation and ultimately cellular apoptosis. On the A subunit &lt;scene name='Shiga_toxin_1/Active_site_zoomed_in/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> <br /> <br /> ==3D structures==<br /> <br /> [[1dm0]] - Stx1&lt;br /&gt;<br /> [[1r4q]] - Stx2&lt;br /&gt;<br /> [[1r4p]] - Stx2 bound to ligand&lt;br /&gt;<br /> [[2ga4]] - Stx2 with adenine&lt;br /&gt;<br /> <br /> '''Mutants'''<br /> <br /> [[1c48]] - Shiga-like toxin B subunit&lt;br /&gt;<br /> [[1cqf]] - Shiga-like toxin B subunit bound to trisaccharide&lt;br /&gt;<br /> [[1bos]] - Shiga-like toxin bound to receptor&lt;br /&gt;<br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1313894 2011-11-07T02:36:04Z

<p>Max Evoy-Mount: </p> <hr /> <div>==Introduction==<br /> '''Shiga Toxins''' are a family of [http://en.wikipedia.org/wiki/AB5_toxin AB5] toxins (Stx1 and Stx2) which cause dysentery, hemolytic-uremic syndrome, and potentially renal failure in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; and shigella dysentarie. STECs are one of the major foodborne pathogens, affecting both developed and third-world countries. The stx gene is not endogenous to these strains, but is introduced through horizontal gene transfer from environmental prophages of the lambdoid bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; Shiga Toxins are closely related to [[ricin]], which is structurally and mechanistically similar. Shiga toxin acts to inhibit protein synthesis in eukaryotic cells and is the main virulence factor of STEC. <br /> <br /> {{STRUCTURE_2ga4| PDB=2ga4 | SCENE= }}<br /> <br /> {{STRUCTURE_1dm0| PDB=1dm0 | SCENE= }}<br /> <br /> ==Human Interaction==<br /> 0157:H7 STECs are spread to humans through a fecal-oral mechanism, primarily from ingestion of food contaminated with fecal material. Cattle, goats, and sheep are the primary reservoir of STECs and their close proximity to food sources as well as the use of animal feces for fertilizer makes them the main route of contamination.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; Inadequate sanitation and contamination of meat during slaughter can both lead to STEC contaminated food at the market. Once ingested the STEC can survive the high acid environment of the stomach and progress to the gut where they attach firmly to gut mucosa via the [http://en.wikipedia.org/wiki/Intimin intimin adhesin protein].&lt;ref name=Russel&gt;PMID: 11321582&lt;/ref&gt; Secreted Stx then either attacks gut epithelia or passes into the bloodstream where it can damage kidney and brain tissue. <br /> <br /> '''Treatments'''<br /> <br /> Treatment with antibiotics is contraindicated as antibiotic treatment has been demonstrated to increase Stx production up to one hundred fold.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; This results from the link between Stx production (and phage induction) to the [http://en.wikipedia.org/wiki/SOS_response SOS response pathway].&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; In the event of renal failure kidney dialysis may be employed. A number of potential treatments are under development including B subunit inhibitors, polysaccharides that promote macrophage uptake of Stx, blocking of the GB3 membrane receptor, and inhibition of [http://en.wikipedia.org/wiki/Retrograde_transport#Retrograde_transport retrograde transport].&lt;ref name=Nishikiwa&gt;PMID: 21644029&lt;/ref&gt;<br /> <br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an AB5 hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The &lt;scene name='Shiga_toxin/B_subunits/1'&gt;5 subunit B pentamer&lt;/scene&gt; interacts with the &lt;scene name='Shiga_toxin/A_subunits/1'&gt;two separate A subunits&lt;/scene&gt; via a <br /> &lt;scene name='Shiga_toxin/A-b_interaction/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The &lt;scene name='Shiga_toxin_1/Active_site_zoomed_out_a-b/1'&gt;glycosidase active site&lt;/scene&gt; is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to globo series glycolipid globotriaosylceramide (Gb3), a eukaryotic membrane receptor, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit.&lt;ref name=Lenz&gt;PMID: 2170899&lt;/ref&gt; Once the A subunit is transported to the cytosol it acts by depurinating the 28S ribosomal RNA which leads to inhibition of protein elongation and ultimately cellular apoptosis. On the A subunit &lt;scene name='Shiga_toxin/Active_site/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> <br /> <br /> ==3D structures==<br /> <br /> [[1dm0]] - Stx1&lt;br /&gt;<br /> [[1r4q]] - Stx2&lt;br /&gt;<br /> [[1r4p]] - Stx2 bound to ligand&lt;br /&gt;<br /> [[2ga4]] - Stx2 with adenine&lt;br /&gt;<br /> <br /> '''Mutants'''<br /> <br /> [[1c48]] - Shiga-like toxin B subunit&lt;br /&gt;<br /> [[1cqf]] - Shiga-like toxin B subunit bound to trisaccharide&lt;br /&gt;<br /> [[1bos]] - Shiga-like toxin bound to receptor&lt;br /&gt;<br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1313874 2011-11-07T01:10:59Z

<p>Max Evoy-Mount: </p> <hr /> <div>==Introduction==<br /> '''Shiga Toxins''' are a family of [http://en.wikipedia.org/wiki/AB5_toxin AB5] toxins (Stx1 and Stx2) which cause dysentery, hemolytic-uremic syndrome, and potentially renal failure in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; and shigella dysentarie. STECs are one of the major foodborne pathogens, affecting both developed and third-world countries. The stx gene is not endogenous to these strains, but is introduced through horizontal gene transfer from environmental prophages of the lambdoid bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; Shiga Toxins are closely related to [[ricin]], which is structurally and mechanistically similar. Shiga toxin acts to inhibit protein synthesis in eukaryotic cells and is the main virulence factor of STEC. <br /> <br /> {{STRUCTURE_2ga4| PDB=2ga4 | SCENE= }}<br /> <br /> {{STRUCTURE_1dm0| PDB=1dm0 | SCENE= }}<br /> <br /> ==Human Interaction==<br /> 0157:H7 STECs are spread to humans through a fecal-oral mechanism, primarily from ingestion of food contaminated with fecal material. Cattle, goats, and sheep are the primary reservoir of STECs and their close proximity to food sources as well as the use of animal feces for fertilizer makes them the main route of contamination.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; Inadequate sanitation and contamination of meat during slaughter can both lead to STEC contaminated food at the market. Once ingested the STEC can survive the high acid environment of the stomach and progress to the gut where they attach firmly to gut mucosa via the [http://en.wikipedia.org/wiki/Intimin intimin adhesin protein].&lt;ref name=Russel&gt;PMID: 11321582&lt;/ref&gt; Secreted Stx then either attacks gut epithelia or passes into the bloodstream where it can damage kidney and brain tissue. <br /> <br /> '''Treatments'''<br /> <br /> Treatment with antibiotics is contraindicated as antibiotic treatment has been demonstrated to increase Stx production up to one hundred fold.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; This results from the link between Stx production (and phage induction) to the [http://en.wikipedia.org/wiki/SOS_response SOS response pathway].&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; In the event of renal failure kidney dialysis may be employed. A number of potential treatments are under development including B subunit inhibitors, polysaccharides that promote macrophage uptake of Stx, blocking of the GB3 membrane receptor, and inhibition of [http://en.wikipedia.org/wiki/Retrograde_transport#Retrograde_transport retrograde transport].&lt;ref name=Nishikiwa&gt;PMID: 21644029&lt;/ref&gt;<br /> <br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an AB5 hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The &lt;scene name='Shiga_toxin/B_subunits/1'&gt;5 subunit B pentamer&lt;/scene&gt; interacts with the &lt;scene name='Shiga_toxin/A_subunits/1'&gt;two separate A subunits&lt;/scene&gt; via a <br /> &lt;scene name='Shiga_toxin/A-b_interaction/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The glycosidase active site is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to globo series glycolipid globotriaosylceramide (Gb3), a eukaryotic membrane receptor, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit.&lt;ref name=Lenz&gt;PMID: 2170899&lt;/ref&gt; Once the A subunit is transported to the cytosol it acts by depurinating the 28S ribosomal RNA which leads to inhibition of protein elongation and ultimately cellular apoptosis. On the A subunit &lt;scene name='Shiga_toxin/Active_site/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> <br /> <br /> ==3D structures==<br /> <br /> [[1dm0]] - Stx1&lt;br /&gt;<br /> [[1r4q]] - Stx2&lt;br /&gt;<br /> [[1r4p]] - Stx2 bound to ligand&lt;br /&gt;<br /> [[2ga4]] - Stx2 with adenine&lt;br /&gt;<br /> <br /> '''Mutants'''<br /> <br /> [[1c48]] - Shiga-like toxin B subunit&lt;br /&gt;<br /> [[1cqf]] - Shiga-like toxin B subunit bound to trisaccharide&lt;br /&gt;<br /> [[1bos]] - Shiga-like toxin bound to receptor&lt;br /&gt;<br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1313860 2011-11-07T00:37:06Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;Structure load='1R4Q' size='500' frame='true' align='right' caption='Shiga Toxin Type 2 (Stx2)'/&gt;<br /> <br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of [http://en.wikipedia.org/wiki/AB5_toxin AB5] toxins (Stx1 and Stx2) which cause dysentery, hemolytic-uremic syndrome, and potentially renal failure in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; and shigella dysentarie. STECs are one of the major foodborne pathogens, affecting both developed and third-world countries. The stx gene is not endogenous to these strains, but is introduced through horizontal gene transfer from environmental prophages of the lambdoid bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; Shiga Toxins are closely related to [[ricin]], which is structurally and mechanistically similar. Shiga toxin acts to inhibit protein synthesis in eukaryotic cells and is the main virulence factor of STEC. <br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an AB5 hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The &lt;scene name='Shiga_toxin/B_subunits/1'&gt;5 subunit B pentamer&lt;/scene&gt; interacts with the &lt;scene name='Shiga_toxin/A_subunits/1'&gt;two separate A subunits&lt;/scene&gt; via a <br /> &lt;scene name='Shiga_toxin/A-b_interaction/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The glycosidase active site is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to globo series glycolipid globotriaosylceramide (Gb3), a eukaryotic membrane receptor, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit.&lt;ref name=Lenz&gt;PMID: 2170899&lt;/ref&gt; Once the A subunit is transported to the cytosol it acts by depurinating the 28S ribosomal RNA which leads to inhibition of protein elongation and ultimately cellular apoptosis. On the A subunit &lt;scene name='Shiga_toxin/Active_site/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> <br /> ==Human Interaction==<br /> 0157:H7 STECs are spread to humans through a fecal-oral mechanism, primarily from ingestion of food contaminated with fecal material. Cattle, goats, and sheep are the primary reservoir of STECs and their close proximity to food sources as well as the use of animal feces for fertilizer makes them the main route of contamination.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; Inadequate sanitation and contamination of meat during slaughter can both lead to STEC contaminated food at the market. Once ingested the STEC can survive the high acid environment of the stomach and progress to the gut where they attach firmly to gut mucosa via the [http://en.wikipedia.org/wiki/Intimin intimin adhesin protein].&lt;ref name=Russel&gt;PMID: 11321582&lt;/ref&gt; Secreted Stx then either attacks gut epithelia or passes into the bloodstream where it can damage kidney and brain tissue. <br /> <br /> '''Treatments'''<br /> <br /> Treatment with antibiotics is contraindicated as antibiotic treatment has been demonstrated to increase Stx production up to one hundred fold.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; This results from the link between Stx production (and phage induction) to the [http://en.wikipedia.org/wiki/SOS_response SOS response pathway].&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; In the event of renal failure kidney dialysis may be employed. A number of potential treatments are under development including B subunit inhibitors, polysaccharides that promote macrophage uptake of Stx, blocking of the GB3 membrane receptor, and inhibition of [http://en.wikipedia.org/wiki/Retrograde_transport#Retrograde_transport retrograde transport].&lt;ref name=Nishikiwa&gt;PMID: 21644029&lt;/ref&gt; <br /> <br /> ==3D structures==<br /> <br /> [[1dm0]] - Stx1&lt;br /&gt;<br /> [[1r4q]] - Stx2&lt;br /&gt;<br /> [[1r4p]] - Stx2 bound to ligand&lt;br /&gt;<br /> [[2ga4]] - Stx2 with adenine&lt;br /&gt;<br /> <br /> '''Mutants'''<br /> <br /> [[1c48]] - Shiga-like toxin B subunit&lt;br /&gt;<br /> [[1cqf]] - Shiga-like toxin B subunit bound to trisaccharide&lt;br /&gt;<br /> [[1bos]] - Shiga-like toxin bound to receptor&lt;br /&gt;<br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1313766 2011-11-04T23:38:03Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;Structure load='1R4Q' size='500' frame='true' align='right' caption='Shiga Toxin Type 2 (Stx2)'/&gt;<br /> <br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of [http://en.wikipedia.org/wiki/AB5_toxin AB5] toxins (Stx1 and Stx2) which cause dysentery, hemolytic-uremic syndrome, and potentially renal failure in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; and shigella dysentarie. STECs are one of the major foodborne pathogens, affecting both developed and third-world countries. The stx gene is not endogenous to these strains, but is introduced through horizontal gene transfer from environmental prophages of the lambdoid bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; Shiga Toxins are closely related to [[ricin]], which is structurally and mechanistically similar. Shiga toxin acts to inhibit protein synthesis in eukaryotic cells and is the main virulence factor of STEC. <br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an AB5 hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The &lt;scene name='Shiga_toxin/B_subunits/1'&gt;5 subunit B pentamer&lt;/scene&gt; interacts with the &lt;scene name='Shiga_toxin/A_subunits/1'&gt;two separate A subunits&lt;/scene&gt; via a <br /> &lt;scene name='Shiga_toxin/A-b_interaction/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The glycosidase active site is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to globo series glycolipid globotriaosylceramide (Gb3), a eukaryotic membrane receptor, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit.&lt;ref name=Lenz&gt;PMID: 2170899&lt;/ref&gt; Once the A subunit is transported to the cytosol it acts by depurinating the 28S ribosomal RNA which leads to inhibition of protein elongation and ultimately cellular apoptosis. On the A subunit &lt;scene name='Shiga_toxin/Active_site/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> <br /> ==Human Interaction==<br /> 0157:H7 STECs are spread to humans through a fecal-oral mechanism, primarily from ingestion of food contaminated with fecal material. Cattle, goats, and sheep are the primary reservoir of STECs and their close proximity to food sources as well as the use of animal feces for fertilizer makes them the main route of contamination.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; Inadequate sanitation and contamination of meat during slaughter can both lead to STEC contaminated food at the market. Once ingested the STEC can survive the high acid environment of the stomach and progress to the gut where they attach firmly to gut mucosa via the [http://en.wikipedia.org/wiki/Intimin intimin adhesin protein].&lt;ref name=Russel&gt;PMID: 11321582&lt;/ref&gt; Secreted Stx then either attacks gut epithelia or passes into the bloodstream where it can damage kidney and brain tissue. <br /> <br /> '''Treatments'''<br /> Treatment with antibiotics is contraindicated as antibiotic treatment has been demonstrated to increase Stx production up to one hundred fold.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; This results from the link between Stx production (and phage induction) to the [http://en.wikipedia.org/wiki/SOS_response SOS response pathway].&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; In the event of renal failure kidney dialysis may be employed. A number of potential treatments are under development including B subunit inhibitors, polysaccharides that promote macrophage uptake of Stx, blocking of the GB3 membrane receptor, and inhibition of [http://en.wikipedia.org/wiki/Retrograde_transport#Retrograde_transport retrograde transport].&lt;ref name=Nishikiwa&gt;PMID: 21644029&lt;/ref&gt; <br /> <br /> ==3D structures==<br /> <br /> [[1dm0]] - Stx1&lt;br /&gt;<br /> [[1r4q]] - Stx2&lt;br /&gt;<br /> [[1r4p]] - Stx2 bound to ligand&lt;br /&gt;<br /> [[2ga4]] - Stx2 with adenine&lt;br /&gt;<br /> <br /> '''Mutants'''<br /> <br /> [[1c48]] - Shiga-like toxin B subunit&lt;br /&gt;<br /> [[1cqf]] - Shiga-like toxin B subunit bound to trisaccharide&lt;br /&gt;<br /> [[1bos]] - Shiga-like toxin bound to receptor&lt;br /&gt;<br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1313763 2011-11-04T23:02:55Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;Structure load='1R4Q' size='500' frame='true' align='right' caption='Shiga Toxin Type 2 (Stx2)'/&gt;<br /> <br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of [http://en.wikipedia.org/wiki/AB5_toxin AB5] toxins (Stx1 and Stx2) which cause dysentery, hemolytic-uremic syndrome, and potentially renal failure in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; and shigella dysentarie. STECs are one of the major foodborne pathogens, affecting both developed and third-world countries. The stx gene is not endogenous to these strains, but is introduced through horizontal gene transfer from environmental prophages of the lambdoid bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; Shiga Toxins are closely related to [[ricin]], which is structurally and mechanistically similar. Shiga toxin acts to inhibit protein synthesis in eukaryotic cells and is the main virulence factor of STEC. <br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an AB5 hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The &lt;scene name='Shiga_toxin/B_subunits/1'&gt;5 subunit B pentamer&lt;/scene&gt; interacts with the &lt;scene name='Shiga_toxin/A_subunits/1'&gt;two separate A subunits&lt;/scene&gt; via a <br /> &lt;scene name='Shiga_toxin/A-b_interaction/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The glycosidase active site is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to globo series glycolipid globotriaosylceramide (Gb3), a eukaryotic membrane receptor, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit.&lt;ref name=Lenz&gt;PMID: 2170899&lt;/ref&gt; Once the A subunit is transported to the cytosol it acts by depurinating the 32S ribosomal RNA which leads to inhibition of protein elongation and ultimately cellular apoptosis. On the A subunit &lt;scene name='Shiga_toxin/Active_site/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> <br /> ==Human Interaction==<br /> 0157:H7 STECs are spread to humans through a fecal-oral mechanism, primarily from ingestion of food contaminated with fecal material. Cattle, goats, and sheep are the primary reservoir of STECs and their close proximity to food sources as well as the use of animal feces for fertilizer makes them the main route of contamination.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; Inadequate sanitation and contamination of meat during slaughter can both lead to STEC contaminated food at the market. Once ingested the STEC can survive the high acid environment of the stomach and progress to the gut where they attach firmly to gut mucosa via the [http://en.wikipedia.org/wiki/Intimin intimin adhesin protein].<br /> <br /> Treatment with antibiotics is contraindicated as antibiotic treatment has been demonstrated to increase Stx production up to one hundred fold.&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; This results from the link between Stx production (and phage induction) to the [http://en.wikipedia.org/wiki/SOS_response SOS response pathway].&lt;ref name=Herold&gt;PMID: 15493821&lt;/ref&gt; <br /> <br /> ==3D structures==<br /> <br /> [[1dm0]] - Stx1&lt;br /&gt;<br /> [[1r4q]] - Stx2&lt;br /&gt;<br /> [[1r4p]] - Stx2 bound to ligand&lt;br /&gt;<br /> [[2ga4]] - Stx2 with adenine&lt;br /&gt;<br /> <br /> '''Mutants'''<br /> <br /> [[1c48]] - Shiga-like toxin B subunit&lt;br /&gt;<br /> [[1cqf]] - Shiga-like toxin B subunit bound to trisaccharide&lt;br /&gt;<br /> [[1bos]] - Shiga-like toxin bound to receptor&lt;br /&gt;<br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=User:Max_Evoy-Mount&diff=1313713 2011-11-03T22:04:46Z

<p>Max Evoy-Mount: </p> <hr /> <div>Senior in Microbiology at UCSB<br /> <br /> The page for Shiga Toxin 1 was constructed for Dr. Duane Sears' course MCDB 108AL (protein lab) at University California Santa Barbara</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1304655 2011-10-21T00:14:54Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;Structure load='1R4Q' size='500' frame='true' align='right' caption='Shiga Toxin Type 2 (Stx2)'/&gt;<br /> <br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of [http://en.wikipedia.org/wiki/AB5_toxin AB5] toxins (Stx1 and Stx2) which cause dysentery and hemolytic-uremic syndrome in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; STEC's are one of the major foodborne pathogens, affecting both developed and third-world countries. The stx gene is not endogenous to these strains, but is introduced by environmental prophages of the lambda bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; Shiga Toxins are closely related to [[ricin]], which is structurally and mechanistically similar. Shiga toxin acts to inhibit protein synthesis in eukaryotic cells and is the main virulence factor of STEC. <br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an AB5 hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The &lt;scene name='Shiga_toxin/B_subunits/1'&gt;5 subunit B pentamer&lt;/scene&gt; interacts with the &lt;scene name='Shiga_toxin/A_subunits/1'&gt;two separate A subunits&lt;/scene&gt; via a <br /> &lt;scene name='Shiga_toxin/A-b_interaction/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The glycosidase active site is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to eukaryotic cell surface, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit. On the A subunit &lt;scene name='Shiga_toxin/Active_site/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> <br /> ==3D structures==<br /> <br /> [[1dm0]] - Stx1&lt;br /&gt;<br /> [[1r4q]] - Stx2&lt;br /&gt;<br /> [[1r4p]] - Stx2 bound to ligand&lt;br /&gt;<br /> [[2ga4]] - Stx2 with adenine&lt;br /&gt;<br /> <br /> '''Mutants'''<br /> <br /> [[1c48]] - Shiga-like toxin B subunit&lt;br /&gt;<br /> [[1cqf]] - Shiga-like toxin B subunit bound to trisaccharide&lt;br /&gt;<br /> [[1bos]] - Shiga-like toxin bound to receptor&lt;br /&gt;<br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1304586 2011-10-18T22:44:27Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;Structure load='1R4Q' size='500' frame='true' align='right' caption='Shiga Toxin Type 2 (Stx2)'/&gt;<br /> <br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of [http://en.wikipedia.org/wiki/AB5_toxin AB5] toxins which cause dysentery in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; The stx gene is not endogenous to these strains, but is introduced by environmental prophages of the lambda bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt;<br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an AB5 hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The &lt;scene name='Shiga_toxin/B_subunits/1'&gt;5 subunit B pentamer&lt;/scene&gt; interacts with the &lt;scene name='Shiga_toxin/A_subunits/1'&gt;two separate A subunits&lt;/scene&gt; via a <br /> &lt;scene name='Shiga_toxin/A-b_interaction/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The glycosidase active site is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to eukaryotic cell surface, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit. On the A subunit &lt;scene name='Shiga_toxin/Active_site/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> <br /> ==3D structures==<br /> <br /> [[1dm0]] - Stx1&lt;br /&gt;<br /> [[1r4q]] - Stx2&lt;br /&gt;<br /> [[1r4p]] - Stx2 bound to ligand&lt;br /&gt;<br /> [[2ga4]] - Stx2 with adenine&lt;br /&gt;<br /> <br /> '''Mutants'''<br /> <br /> [[1c48]] - Shiga-like toxin B subunit&lt;br /&gt;<br /> [[1cqf]] - Shiga-like toxin B subunit bound to trisaccharide&lt;br /&gt;<br /> [[1bos]] - Shiga-like toxin bound to receptor&lt;br /&gt;<br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1304583 2011-10-18T22:29:50Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;Structure load='1R4Q' size='500' frame='true' align='right' caption='Shiga Toxin Type 2 (Stx2)'/&gt;<br /> <br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of AB5 toxins which cause dysentery in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; The stx gene is not endogenous to these strains, but is introduced by environmental prophages of the lambda bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt;<br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an [http://en.wikipedia.org/wiki/AB5_toxin AB5] hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The &lt;scene name='Shiga_toxin/B_subunits/1'&gt;5 subunit B pentamer&lt;/scene&gt; interacts with the &lt;scene name='Shiga_toxin/A_subunits/1'&gt;two separate A subunits&lt;/scene&gt; via a <br /> &lt;scene name='Shiga_toxin/A-b_interaction/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The glycosidase active site is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to eukaryotic cell surface, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit. On the A subunit &lt;scene name='Shiga_toxin/Active_site/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> <br /> ==3D structures==<br /> <br /> [[1dm0]] - Stx1&lt;br /&gt;<br /> [[1r4q]] - Stx2&lt;br /&gt;<br /> [[1r4p]] - Stx2 bound to ligand&lt;br /&gt;<br /> [[2ga4]] - Stx2 with adenine&lt;br /&gt;<br /> <br /> '''Mutants'''<br /> <br /> [[1c48]] - Shiga-like toxin B subunit&lt;br /&gt;<br /> [[1cqf]] - Shiga-like toxin B subunit bound to trisaccharide&lt;br /&gt;<br /> [[1bos]] - Shiga-like toxin bound to receptor&lt;br /&gt;<br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1304581 2011-10-18T22:27:26Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;Structure load='1R4Q' size='500' frame='true' align='right' caption='Shiga Toxin Type 2 (Stx2)'/&gt;<br /> <br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of AB5 toxins which cause dysentery in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; The stx gene is not endogenous to these strains, but is introduced by environmental prophages of the lambda bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt;<br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an [http://en.wikipedia.org/wiki/AB5_toxin AB5] hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The &lt;scene name='Shiga_toxin/B_subunits/1'&gt;5 subunit B pentamer&lt;/scene&gt; interacts with the &lt;scene name='Shiga_toxin/A_subunits/1'&gt;two separate A subunits&lt;/scene&gt; via a <br /> &lt;scene name='Shiga_toxin/A-b_interaction/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The glycosidase active site is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to eukaryotic cell surface, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit. On the A subunit &lt;scene name='Shiga_toxin/Active_site/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> <br /> ==3D structures==<br /> <br /> [[1dm0]] - Stx1,br /&gt;<br /> [[1r4q]] - Stx2&lt;br /&gt;<br /> [[1r4p]] - Stx2 bound to ligand&lt;br /&gt;<br /> [[2ga4]] - Stx2 with adenine&lt;br /&gt;<br /> <br /> '''Mutants'''<br /> <br /> [[1c48]] - Shiga-like toxin B subunit&lt;br /&gt;<br /> [[1cqf]] - Shiga-like toxin B subunit bound to trisaccharide&lt;br /&gt;<br /> [[1bos]] - Shiga-like toxin bound to receptor&lt;br /&gt;<br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1304576 2011-10-18T22:10:21Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;Structure load='1R4Q' size='500' frame='true' align='right' caption='Shiga Toxin Type 1 (Stx1)'/&gt;<br /> <br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of AB5 toxins which cause dysentery in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; The stx gene is not endogenous to these strains, but is introduced by environmental prophages of the lambda bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt;<br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an [http://en.wikipedia.org/wiki/AB5_toxin AB5] hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The &lt;scene name='Shiga_toxin/B_subunits/1'&gt;5 subunit B pentamer&lt;/scene&gt; interacts with the &lt;scene name='Shiga_toxin/A_subunits/1'&gt;two separate A subunits&lt;/scene&gt; via a <br /> &lt;scene name='Shiga_toxin/A-b_interaction/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The glycosidase active site is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to eukaryotic cell surface, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit. On the A subunit &lt;scene name='Shiga_toxin/Active_site/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1304481 2011-10-14T23:13:07Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;Structure load='1R4Q' size='500' frame='true' align='right' caption='Shiga Toxin Type 2 (Stx2)'/&gt;<br /> <br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of AB5 toxins which cause dysentery in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; The stx gene is not endogenous to these strains, but is introduced by environmental prophages of the lambda bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt;<br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an [http://en.wikipedia.org/wiki/AB5_toxin AB5] hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The &lt;scene name='Shiga_toxin/B_subunits/1'&gt;5 subunit B pentamer&lt;/scene&gt; interacts with the &lt;scene name='Shiga_toxin/A_subunits/1'&gt;two separate A subunits&lt;/scene&gt; via a <br /> &lt;scene name='Shiga_toxin/A-b_interaction/1'&gt;C-terminal helix of hydrophobic subunits packed antiparallel to 5 B helixes&lt;/scene&gt; and <br /> &lt;scene name='Shiga_toxin_1/Beta_sheet/1'&gt;4 antiparallel beta sheets&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The glycosidase active site is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to eukaryotic cell surface, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit. On the A subunit &lt;scene name='Shiga_toxin/Active_site/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1304463 2011-10-14T05:54:35Z

<p>Max Evoy-Mount: Shiga toxin moved to Shiga toxin 1: Shiga Toxin includes stx1 and stx2; I only want to address stx1</p> <hr /> <div>&lt;Structure load='1R4Q' size='500' frame='true' align='right' caption='Shiga Toxin Type 2 (Stx2)'/&gt;<br /> <br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of AB5 toxins which cause dysentery in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; The stx gene is not endogenous to these strains, but is introduced by environmental prophages of the lambda bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt;<br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an [http://en.wikipedia.org/wiki/AB5_toxin AB5] hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The &lt;scene name='Shiga_toxin/B_subunits/1'&gt;5 subunit B pentamer&lt;/scene&gt; interacts with the &lt;scene name='Shiga_toxin/A_subunits/1'&gt;two separate A subunits&lt;/scene&gt; via a <br /> &lt;scene name='Shiga_toxin/A-b_interaction/1'&gt;C-terminal helix and 4 stranded beta-sheet&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The glycosidase active site is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to eukaryotic cell surface, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit. On the A subunit &lt;scene name='Shiga_toxin/Active_site/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1304462 2011-10-14T04:20:27Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;Structure load='1R4Q' size='500' frame='true' align='right' caption='Shiga Toxin Type 2 (Stx2)'/&gt;<br /> <br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of AB5 toxins which cause dysentery in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; The stx gene is not endogenous to these strains, but is introduced by environmental prophages of the lambda bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt;<br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an [http://en.wikipedia.org/wiki/AB5_toxin AB5] hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The &lt;scene name='Shiga_toxin/B_subunits/1'&gt;5 subunit B pentamer&lt;/scene&gt; interacts with the &lt;scene name='Shiga_toxin/A_subunits/1'&gt;two separate A subunits&lt;/scene&gt; via a <br /> &lt;scene name='Shiga_toxin/A-b_interaction/1'&gt;C-terminal helix and 4 stranded beta-sheet&lt;/scene&gt;.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The glycosidase active site is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to eukaryotic cell surface, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit. On the A subunit &lt;scene name='Shiga_toxin/Active_site/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1304461 2011-10-14T03:37:19Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;Structure load='1R4Q' size='500' frame='true' align='right' caption='Shiga Toxin Type 2 (Stx2)'/&gt;<br /> <br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of AB5 toxins which cause dysentery in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; The stx gene is not endogenous to these strains, but is introduced by environmental prophages of the lambda bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt;<br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an [http://en.wikipedia.org/wiki/AB5_toxin AB5] hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The &lt;scene name='Shiga_toxin/B_subunits/1'&gt;5 subunit B pentamer&lt;/scene&gt; interacts with the &lt;scene name='Shiga_toxin/A_subunits/1'&gt;two separate A subunits&lt;/scene&gt; via a C-terminal helix and 4 stranded beta-sheet.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The glycosidase active site is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to eukaryotic cell surface, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit. On the A subunit &lt;scene name='Shiga_toxin/Active_site/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1304460 2011-10-14T03:31:06Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;Structure load='1R4Q' size='500' frame='true' align='right' caption='Shiga Toxin Type 2 (Stx2)'/&gt;<br /> <br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of AB5 toxins which cause dysentery in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; The stx gene is not endogenous to these strains, but is introduced by environmental prophages of the lambda bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt;<br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an [http://en.wikipedia.org/wiki/AB5_toxin AB5] hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The 5 subunit B pentamer interacts with a &lt;scene name='Shiga_toxin/A_subunits/1'&gt;two separate A subunits&lt;/scene&gt; via a C-terminal helix and 4 stranded beta-sheet.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The glycosidase active site is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to eukaryotic cell surface, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit. On the A subunit &lt;scene name='Shiga_toxin/Active_site/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1304459 2011-10-14T03:22:08Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;Structure load='1R4Q' size='500' frame='true' align='right' caption='Shiga Toxin Type 2 (Stx2)'/&gt;<br /> <br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of AB5 toxins which cause dysentery in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt; The stx gene is not endogenous to these strains, but is introduced by environmental prophages of the lambda bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt;<br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an [http://en.wikipedia.org/wiki/AB5_toxin AB5] hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The 5 subunit B pentamer interacts with a single A subunit via a C-terminal helix and 4 stranded beta-sheet.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;. The glycosidase active site is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt;<br /> <br /> ==Function==<br /> <br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to eukaryotic cell surface, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit. On the A subunit &lt;scene name='Shiga_toxin/Active_site/1'&gt;Tyr77, Tyr114, Glu167, Arg170, and Trp203&lt;/scene&gt; are all essential in glycosidic activity.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; <br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1304458 2011-10-14T02:44:41Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;Structure load='1R4Q' size='500' frame='true' align='right' caption='Shiga Toxin Type 2 (Stx2)'/&gt;<br /> <br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of AB5 toxins which cause dysentery in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain.&lt;ref name=Wagner&gt; The stx gene is not endogenous to these strains, but is introduced by environmental prophages of the lambda bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt;<br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an [http://en.wikipedia.org/wiki/AB5_toxin AB5] hexamer.&lt;ref name=Fraser&gt;PMID: 7656009&lt;/ref&gt; The 5 subunit B pentamer interacts with a single A subunit via a C-terminal helix and 4 stranded beta-sheet.&lt;ref name=Fraser&gt; The glycosidase active site is located on the A subunit, but is blocked by the B subunit until they are cleaved and an active A subunit is released into the target cell.&lt;ref name=Fraser&gt; <br /> <br /> ==Function==<br /> Shiga Toxin acts as an N-glycosidase, removing an adenine from the 60S ribosomal rRNA of a target cell leading to reduced protein synthesis.&lt;ref name=Di&gt;PMID: 21184769&lt;/ref&gt; The B subunit is necessary for binding to eukaryotic cell surface, where it is then endocytosed and proteolytically cleaved into two active A subunits and a B subunit. On the A subunit Tyr77, Tyr114, Glu167, Arg170, and Trp203 are all essential in glycosidic activity.&lt;ref name=Di&gt; <br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1304457 2011-10-14T01:11:05Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;Structure load='1R4Q' size='500' frame='true' align='right' caption='Shiga Toxin Type 2 (Stx2)'/&gt;<br /> <br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of AB5 toxins which cause dysentery in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain.&lt;ref name=Wagner&gt; The stx gene is not endogenous to these strains, but is introduced by environmental prophages of the lambda bacteriophage family and incorporated into the E. Coli genome.&lt;ref name=Wagner&gt;PMID: 12010491&lt;/ref&gt;<br /> <br /> ==Structure==<br /> Shiga Toxin consists consists of an [http://en.wikipedia.org/wiki/AB5_toxin AB5] hexamer, by X-ray crystallography. The five B subunits form a pentameric ring, encircling a helix at the carboxy terminus of the A subunit. The A subunit interacts with the B pentamer via this C-terminal helix and a four-stranded mixed beta-sheet. The fold of the rest of the A subunit is similar to that of the A chain of the plant toxin ricin; both are N-glycosidases. However, the active site in the bacterial holotoxin is blocked by a segment of polypeptide chain. These residues of the A subunit would be released as part of the activation mechanism of the toxin. <br /> <br /> ==References==<br /> {{Reflist}}</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1304455 2011-10-13T21:09:50Z

<p>Max Evoy-Mount: </p> <hr /> <div>&lt;Structure load='1R4Q' size='500' frame='true' align='right' caption='Shiga Toxin Type 2 (Stx2)'/&gt;<br /> <br /> ==Introduction==<br /> '''Shiga Toxins''' are a family of AB5 toxins which cause dysentery in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain. The stx gene is not endogenous to these strains, but introduced by environmental prophages of the lambda bacteriophage family and incorporated into the E. Coli genome[[1]]. <br /> <br /> <br /> ==Citations==<br /> [[1]] [http://www.ncbi.nlm.nih.gov/pubmed/12010491 Bacteriophage control of Shiga Toxin 1 production and release by Escherichia coli]</div>

Max Evoy-Mount https://proteopedia.org/index.php?title=Shiga_toxin&diff=1304454 2011-10-13T21:02:25Z

<p>Max Evoy-Mount: Starting Out</p> <hr /> <div>&lt;Structure load='1R4Q' size='500' frame='true' align='right' caption='Shiga Toxin Type 2 (Stx2)' scene='Insert optional scene name here' /&gt;&lt;!-- <br /> <br /> == Introduction ==<br /> '''Shiga Toxins''' are a family of AB5 toxins which cause dysentery in humans. They are primarily secreted by Shiga toxin-encoding Escherichia coli (STEC), notably by the 0157:H7 strain. The stx gene is not endogenous to these strains, but introduced by environmental prophages of the lambda bacteriophage family and incorporated into the E. Coli genome[[1]]. <br /> <br /> <br /> == Citations ==<br /> [[1]] [http://www.ncbi.nlm.nih.gov/pubmed/12010491 Bacteriophage control of Shiga Toxin 1 production and release by Escherichia coli]</div>

Max Evoy-Mount