2k9r

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Current revision (06:09, 27 November 2024) (edit) (undo)
 
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==Enhancing the activity of insulin by stereospecific unfolding==
==Enhancing the activity of insulin by stereospecific unfolding==
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<StructureSection load='2k9r' size='340' side='right'caption='[[2k9r]], [[NMR_Ensembles_of_Models | 20 NMR models]]' scene=''>
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<StructureSection load='2k9r' size='340' side='right'caption='[[2k9r]]' scene=''>
== Structural highlights ==
== Structural highlights ==
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<table><tr><td colspan='2'>[[2k9r]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2K9R OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2K9R FirstGlance]. <br>
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<table><tr><td colspan='2'>[[2k9r]] 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=2K9R OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2K9R FirstGlance]. <br>
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</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>
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</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>
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<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[2k91|2k91]]</div></td></tr>
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<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>
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<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">INS ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=2k9r FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2k9r OCA], [https://pdbe.org/2k9r PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2k9r RCSB], [https://www.ebi.ac.uk/pdbsum/2k9r PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2k9r ProSAT]</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=2k9r FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2k9r OCA], [https://pdbe.org/2k9r PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2k9r RCSB], [https://www.ebi.ac.uk/pdbsum/2k9r PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2k9r ProSAT]</span></td></tr>
</table>
</table>
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== Disease ==
 
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[[https://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Defects in INS are the cause of familial hyperproinsulinemia (FHPRI) [MIM:[https://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:[https://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:[https://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:[https://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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[[https://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.
 
== Evolutionary Conservation ==
== Evolutionary Conservation ==
[[Image:Consurf_key_small.gif|200px|right]]
[[Image:Consurf_key_small.gif|200px|right]]
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<jmolCheckbox>
<jmolCheckbox>
<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/k9/2k9r_consurf.spt"</scriptWhenChecked>
<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/k9/2k9r_consurf.spt"</scriptWhenChecked>
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<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
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<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview03.spt</scriptWhenUnchecked>
<text>to colour the structure by Evolutionary Conservation</text>
<text>to colour the structure by Evolutionary Conservation</text>
</jmolCheckbox>
</jmolCheckbox>
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__TOC__
__TOC__
</StructureSection>
</StructureSection>
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[[Category: Human]]
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[[Category: Homo sapiens]]
[[Category: Large Structures]]
[[Category: Large Structures]]
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[[Category: Hu, S Q]]
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[[Category: Hu SQ]]
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[[Category: Hua, Q X]]
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[[Category: Hua QX]]
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[[Category: Huang, K]]
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[[Category: Huang K]]
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[[Category: Jia, W H]]
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[[Category: Jia WH]]
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[[Category: Katsoyannis, P G]]
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[[Category: Katsoyannis PG]]
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[[Category: Nakarawa, S]]
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[[Category: Nakarawa S]]
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[[Category: Philips, N F.P]]
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[[Category: Philips NFP]]
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[[Category: Weiss, M A]]
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[[Category: Weiss MA]]
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[[Category: Wittaker, J]]
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[[Category: Wittaker J]]
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[[Category: Wittaker, L]]
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[[Category: Wittaker L]]
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[[Category: Xu, B]]
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[[Category: Xu B]]
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[[Category: Carbohydrate metabolism]]
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[[Category: Cleavage on pair of basic residue]]
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[[Category: Diabetes mellitus]]
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[[Category: Disease mutation]]
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[[Category: Glucose metabolism]]
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[[Category: Hormone]]
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[[Category: Insulin]]
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[[Category: Mutant]]
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[[Category: Pharmaceutical]]
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[[Category: Secreted]]
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Current revision

Enhancing the activity of insulin by stereospecific unfolding

PDB ID 2k9r

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