2o2l: Difference between revisions

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==Overview==

In a number of bacterial infections, such as Helicobacter pylori, Campylobacter jejuni and Vibrio cholerae infections, a correlation between, the severity of disease and blood group phenotype of infected individuals, has been observed. In the present investigation, we have studied the, molecular basis of this effect for enterotoxigenic Escherichia coli (ETEC), infections. ETEC are non-invasive bacteria, which act through second, messenger pathways to cause diarrhea. It has been suggested that the major, virulence factor of ETEC from human isolates, i.e. the human heat-labile, enterotoxin (hLT), recognizes certain blood group epitopes, although the, molecular basis of blood group antigen recognition is unknown. The 2.5 A, crystal structure of the receptor-binding B-subunit of hLT in complex with, the blood group A antigen analog, GalNAcalpha3(Fucalpha2)Galbeta4(Fucalpha3)Glcbeta provides evidence of a, previously unknown binding site in the native toxin. The structure reveals, the molecular interactions underlying blood group antigen recognition and, suggests how this protein can discriminate between different blood group, epitopes. These results support the previously debated role of hLT in the, blood group dependence of ETEC infections. Similar observations regarding, the closely related cholera toxin in V. cholera infections are also, discussed.

In a number of bacterial infections, such as Helicobacter pylori, Campylobacter jejuni and Vibrio cholerae infections, a correlation between the severity of disease and blood group phenotype of infected individuals has been observed. In the present investigation, we have studied the molecular basis of this effect for enterotoxigenic Escherichia coli (ETEC) infections. ETEC are non-invasive bacteria, which act through second messenger pathways to cause diarrhea. It has been suggested that the major virulence factor of ETEC from human isolates, i.e. the human heat-labile enterotoxin (hLT), recognizes certain blood group epitopes, although the molecular basis of blood group antigen recognition is unknown. The 2.5 A crystal structure of the receptor-binding B-subunit of hLT in complex with the blood group A antigen analog GalNAcalpha3(Fucalpha2)Galbeta4(Fucalpha3)Glcbeta provides evidence of a previously unknown binding site in the native toxin. The structure reveals the molecular interactions underlying blood group antigen recognition and suggests how this protein can discriminate between different blood group epitopes. These results support the previously debated role of hLT in the blood group dependence of ETEC infections. Similar observations regarding the closely related cholera toxin in V. cholera infections are also discussed.

==About this Structure==

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==Reference==

Blood ~~Group Antigen Recognition~~ by Escherichia coli ~~Heat~~-labile ~~Enterotoxin~~., Holmner A, Askarieh G, Okvist M, Krengel U, J Mol Biol. 2007 Aug 17;371(3):754-64. Epub 2007 May 31. PMID:[http://ispc.weizmann.ac.il//pmbin/getpm?pmid=17586525 17586525]

Blood group antigen recognition by Escherichia coli heat-labile enterotoxin., Holmner A, Askarieh G, Okvist M, Krengel U, J Mol Biol. 2007 Aug 17;371(3):754-64. Epub 2007 May 31. PMID:[http://ispc.weizmann.ac.il//pmbin/getpm?pmid=17586525 17586525]

[[Category: Escherichia coli]]

[[Category: Single protein]]

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[[Category: heat-labile enterotoxin]]

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@@ Line 4: / Line 4: @@
 ==Overview==
-In a number of bacterial infections, such as Helicobacter pylori, Campylobacter jejuni and Vibrio cholerae infections, a correlation between, the severity of disease and blood group phenotype of infected individuals, has been observed. In the present investigation, we have studied the, molecular basis of this effect for enterotoxigenic Escherichia coli (ETEC), infections. ETEC are non-invasive bacteria, which act through second, messenger pathways to cause diarrhea. It has been suggested that the major, virulence factor of ETEC from human isolates, i.e. the human heat-labile, enterotoxin (hLT), recognizes certain blood group epitopes, although the, molecular basis of blood group antigen recognition is unknown. The 2.5 A, crystal structure of the receptor-binding B-subunit of hLT in complex with, the blood group A antigen analog, GalNAcalpha3(Fucalpha2)Galbeta4(Fucalpha3)Glcbeta provides evidence of a, previously unknown binding site in the native toxin. The structure reveals, the molecular interactions underlying blood group antigen recognition and, suggests how this protein can discriminate between different blood group, epitopes. These results support the previously debated role of hLT in the, blood group dependence of ETEC infections. Similar observations regarding, the closely related cholera toxin in V. cholera infections are also, discussed.
+In a number of bacterial infections, such as Helicobacter pylori, Campylobacter jejuni and Vibrio cholerae infections, a correlation between the severity of disease and blood group phenotype of infected individuals has been observed. In the present investigation, we have studied the molecular basis of this effect for enterotoxigenic Escherichia coli (ETEC) infections. ETEC are non-invasive bacteria, which act through second messenger pathways to cause diarrhea. It has been suggested that the major virulence factor of ETEC from human isolates, i.e. the human heat-labile enterotoxin (hLT), recognizes certain blood group epitopes, although the molecular basis of blood group antigen recognition is unknown. The 2.5 A crystal structure of the receptor-binding B-subunit of hLT in complex with the blood group A antigen analog GalNAcalpha3(Fucalpha2)Galbeta4(Fucalpha3)Glcbeta provides evidence of a previously unknown binding site in the native toxin. The structure reveals the molecular interactions underlying blood group antigen recognition and suggests how this protein can discriminate between different blood group epitopes. These results support the previously debated role of hLT in the blood group dependence of ETEC infections. Similar observations regarding the closely related cholera toxin in V. cholera infections are also discussed.
 ==About this Structure==
@@ Line 10: / Line 10: @@
 ==Reference==
-Blood Group Antigen Recognition by Escherichia coli Heat-labile Enterotoxin., Holmner A, Askarieh G, Okvist M, Krengel U, J Mol Biol. 2007 Aug 17;371(3):754-64. Epub 2007 May 31. PMID:[http://ispc.weizmann.ac.il//pmbin/getpm?pmid=17586525 17586525]
+Blood group antigen recognition by Escherichia coli heat-labile enterotoxin., Holmner A, Askarieh G, Okvist M, Krengel U, J Mol Biol. 2007 Aug 17;371(3):754-64. Epub 2007 May 31. PMID:[http://ispc.weizmann.ac.il//pmbin/getpm?pmid=17586525 17586525]
 [[Category: Escherichia coli]]
 [[Category: Single protein]]
@@ Line 21: / Line 21: @@
 [[Category: heat-labile enterotoxin]]
-''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Jan 23 13:42:50 2008''
+''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Thu Feb 21 18:13:43 2008''