5uqa: Difference between revisions

Line 1:

~~'''Unreleased structure'''~~

~~The~~ entry ~~5uqa~~ is ~~ON HOLD~~ ~~until Paper Publication~~

==Insulin with proline analog FzP at position B28 in the R6 state==

~~Authors~~:

== Structural highlights ==

<table><tr><td colspan='2'>[[5uqa]] is a 12 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5UQA OCA]. For a guided tour on the structure components use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5UQA FirstGlance].

~~Description~~:

</td></tr><tr id='ligand'><td class="sblockLbl">[[Ligand|Ligands:]]</td><td class="sblockDat"><scene name='pdbligand=ACN:ACETONE'>ACN</scene>, <scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=NA:SODIUM+ION'>NA</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>

[[Category: ~~Unreleased Structures~~]]

<tr id='NonStdRes'><td class="sblockLbl">[[Non-Standard_Residue|NonStd Res:]]</td><td class="sblockDat"><scene name='pdbligand=4FB:(4S)-4-FLUORO-L-PROLINE'>4FB</scene></td></tr>

<tr id='resources'><td class="sblockLbl">Resources:</td><td class="sblockDat">[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5uqa FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5uqa OCA], [http://pdbe.org/5uqa PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5uqa RCSB], [http://www.ebi.ac.uk/pdbsum/5uqa PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5uqa ProSAT]</td></tr>

</table>

== Disease ==

[[http://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Defects in INS are the cause of familial hyperproinsulinemia (FHPRI) [MIM:[http://omim.org/entry/176730 176730]].<ref>PMID:3470784</ref> <ref>PMID:2196279</ref> <ref>PMID:4019786</ref> <ref>PMID:1601997</ref> Defects in INS are a cause of diabetes mellitus insulin-dependent type 2 (IDDM2) [MIM:[http://omim.org/entry/125852 125852]]. IDDM2 is a multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Clinical fetaures are polydipsia, polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.<ref>PMID:18192540</ref> Defects in INS are a cause of diabetes mellitus permanent neonatal (PNDM) [MIM:[http://omim.org/entry/606176 606176]]. PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy.<ref>PMID:17855560</ref> <ref>PMID:18162506</ref> Defects in INS are a cause of maturity-onset diabetes of the young type 10 (MODY10) [MIM:[http://omim.org/entry/613370 613370]]. MODY10 is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.<ref>PMID:18192540</ref> <ref>PMID:18162506</ref> <ref>PMID:20226046</ref>

== Function ==

[[http://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver.

== References ==

__TOC__

</StructureSection>

[[Category: Fang, K Y]]

[[Category: Lieblich, S A]]

[[Category: Tirrell, D A]]

[[Category: Hormone]]

[[Category: Insulin hormone]]

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@@ Line 1: / Line 1: @@
-'''Unreleased structure'''
-The entry 5uqa is ON HOLD  until Paper Publication
+==Insulin with proline analog FzP at position B28 in the R6 state==
+<StructureSection load='5uqa' size='340' side='right' caption='[[5uqa]], [[Resolution|resolution]] 1.31&Aring;' scene=''>
-Authors:
+== Structural highlights ==
+<table><tr><td colspan='2'>[[5uqa]] is a 12 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5UQA OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5UQA FirstGlance]. <br>
-Description:
+</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=ACN:ACETONE'>ACN</scene>, <scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=NA:SODIUM+ION'>NA</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
-[[Category: Unreleased Structures]]
+<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=4FB:(4S)-4-FLUORO-L-PROLINE'>4FB</scene></td></tr>
+<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5uqa FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5uqa OCA], [http://pdbe.org/5uqa PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5uqa RCSB], [http://www.ebi.ac.uk/pdbsum/5uqa PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5uqa ProSAT]</span></td></tr>
+</table>
+== Disease ==
+[[http://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Defects in INS are the cause of familial hyperproinsulinemia (FHPRI) [MIM:[http://omim.org/entry/176730 176730]].<ref>PMID:3470784</ref> <ref>PMID:2196279</ref> <ref>PMID:4019786</ref> <ref>PMID:1601997</ref>   Defects in INS are a cause of diabetes mellitus insulin-dependent type 2 (IDDM2) [MIM:[http://omim.org/entry/125852 125852]]. IDDM2 is a multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Clinical fetaures are polydipsia, polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.<ref>PMID:18192540</ref>   Defects in INS are a cause of diabetes mellitus permanent neonatal (PNDM) [MIM:[http://omim.org/entry/606176 606176]]. PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy.<ref>PMID:17855560</ref> <ref>PMID:18162506</ref>   Defects in INS are a cause of maturity-onset diabetes of the young type 10 (MODY10) [MIM:[http://omim.org/entry/613370 613370]]. MODY10 is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.<ref>PMID:18192540</ref> <ref>PMID:18162506</ref> <ref>PMID:20226046</ref>
+== Function ==
+[[http://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver.
+== References ==
+<references/>
+__TOC__
+</StructureSection>
+[[Category: Fang, K Y]]
+[[Category: Lieblich, S A]]
+[[Category: Tirrell, D A]]
+[[Category: Hormone]]
+[[Category: Insulin hormone]]