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| ==NMR Structure of human insulin mutant GLY-B20-D-ALA, GLY-B23-D-ALA PRO-B28-LYS, LYS-B29-PRO, 20 Structures== | | ==NMR Structure of human insulin mutant GLY-B20-D-ALA, GLY-B23-D-ALA PRO-B28-LYS, LYS-B29-PRO, 20 Structures== |
| <StructureSection load='2l1y' size='340' side='right' caption='[[2l1y]], [[NMR_Ensembles_of_Models | 20 NMR models]]' scene=''> | | <StructureSection load='2l1y' size='340' side='right'caption='[[2l1y]]' scene=''> |
| == Structural highlights == | | == Structural highlights == |
| <table><tr><td colspan='2'>[[2l1y]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2L1Y OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2L1Y FirstGlance]. <br> | | <table><tr><td colspan='2'>[[2l1y]] 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=2L1Y OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2L1Y FirstGlance]. <br> |
| </td></tr><tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=DAL:D-ALANINE'>DAL</scene></td></tr> | | </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='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[3oal|3oal]], [[3ob3|3ob3]], [[3ob5|3ob5]], [[2l1z|2l1z]]</td></tr> | | <tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=DAL:D-ALANINE'>DAL</scene></td></tr> |
| <tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">INS ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=2l1y FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2l1y OCA], [https://pdbe.org/2l1y PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2l1y RCSB], [https://www.ebi.ac.uk/pdbsum/2l1y PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2l1y ProSAT]</span></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=2l1y FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2l1y OCA], [http://pdbe.org/2l1y PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2l1y RCSB], [http://www.ebi.ac.uk/pdbsum/2l1y PDBsum]</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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| ==See Also== | | ==See Also== |
| *[[Molecular Playground/Insulin|Molecular Playground/Insulin]] | | *[[Insulin 3D Structures|Insulin 3D Structures]] |
| == References ==
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| <references/>
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| __TOC__ | | __TOC__ |
| </StructureSection> | | </StructureSection> |
| [[Category: Human]] | | [[Category: Homo sapiens]] |
| [[Category: Hu, S Q]] | | [[Category: Large Structures]] |
| [[Category: Hua, Q X]] | | [[Category: Hu SQ]] |
| [[Category: Huang, K]] | | [[Category: Hua QX]] |
| [[Category: Katsoyannis, J W]] | | [[Category: Huang K]] |
| [[Category: Philips, N B]] | | [[Category: Katsoyannis JW]] |
| [[Category: Wan, Z L]] | | [[Category: Philips NB]] |
| [[Category: Weiss, M A]] | | [[Category: Wan ZL]] |
| [[Category: Hormone]]
| | [[Category: Weiss MA]] |
| [[Category: Human insulin]]
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| [[Category: Mutant]]
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