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| {{STRUCTURE_2lgb| PDB=2lgb | SCENE= }}
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| ===Modified A22Gly-B31Arg Human Insulin===
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| ==Disease== | | ==Modified A22Gly-B31Arg Human Insulin== |
| [[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> | | <StructureSection load='2lgb' size='340' side='right'caption='[[2lgb]]' scene=''> |
| | | == Structural highlights == |
| ==Function== | | <table><tr><td colspan='2'>[[2lgb]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2LGB OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2LGB FirstGlance]. <br> |
| [[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.
| | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Solution NMR, 20 models</td></tr> |
| | | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=2lgb FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2lgb OCA], [https://pdbe.org/2lgb PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2lgb RCSB], [https://www.ebi.ac.uk/pdbsum/2lgb PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2lgb ProSAT]</span></td></tr> |
| ==About this Structure== | | </table> |
| [[2lgb]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2LGB OCA].
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| ==See Also== | | ==See Also== |
| *[[Molecular Playground/Insulin|Molecular Playground/Insulin]] | | *[[Insulin 3D Structures|Insulin 3D Structures]] |
| | | __TOC__ |
| ==Reference==
| | </StructureSection> |
| <ref group="xtra">PMID:022350952</ref><references group="xtra"/><references/>
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| [[Category: Homo sapiens]] | | [[Category: Homo sapiens]] |
| [[Category: Bocian, W.]] | | [[Category: Large Structures]] |
| [[Category: Kozerski, L.]] | | [[Category: Bocian W]] |
| [[Category: Hormone]] | | [[Category: Kozerski L]] |
