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| ==Structure of [L-HisB24] insulin analogue at pH 8.0== | | ==Structure of [L-HisB24] insulin analogue at pH 8.0== |
| <StructureSection load='2m2n' size='340' side='right' caption='[[2m2n]], [[NMR_Ensembles_of_Models | 30 NMR models]]' scene=''> | | <StructureSection load='2m2n' size='340' side='right'caption='[[2m2n]]' scene=''> |
| == Structural highlights == | | == Structural highlights == |
| <table><tr><td colspan='2'>[[2m2n]] is a 2 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2M2N OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2M2N FirstGlance]. <br> | | <table><tr><td colspan='2'>[[2m2n]] 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=2M2N OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2M2N FirstGlance]. <br> |
| </td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[2m2m|2m2m]], [[2m2o|2m2o]], [[2m2p|2m2p]]</td></tr> | | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Solution NMR, 30 models</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=2m2n FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2m2n OCA], [http://pdbe.org/2m2n PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2m2n RCSB], [http://www.ebi.ac.uk/pdbsum/2m2n PDBsum]</span></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=2m2n FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2m2n OCA], [https://pdbe.org/2m2n PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2m2n RCSB], [https://www.ebi.ac.uk/pdbsum/2m2n PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2m2n ProSAT]</span></td></tr> |
| </table> | | </table> |
| == Disease ==
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| [[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>
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| == Function ==
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| [[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.
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| <div style="background-color:#fffaf0;"> | | <div style="background-color:#fffaf0;"> |
| == Publication Abstract from PubMed == | | == Publication Abstract from PubMed == |
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| ==See Also== | | ==See Also== |
| *[[Molecular Playground/Insulin|Molecular Playground/Insulin]] | | *[[Insulin 3D Structures|Insulin 3D Structures]] |
| == References == | | == References == |
| <references/> | | <references/> |
| __TOC__ | | __TOC__ |
| </StructureSection> | | </StructureSection> |
| [[Category: Jiracek, J]] | | [[Category: Homo sapiens]] |
| [[Category: Veverka, V]] | | [[Category: Large Structures]] |
| [[Category: Zakova, L]] | | [[Category: Jiracek J]] |
| [[Category: Hormone]] | | [[Category: Veverka V]] |
| [[Category: Insulin]] | | [[Category: Zakova L]] |