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| - | ==Crystal Structure of Insulin in Complex with Sulfatide==
| + | #REDIRECT [[4xc4]] This PDB entry is obsolete and replaced by 4xc4 |
| - | <StructureSection load='3brr' size='340' side='right' caption='[[3brr]], [[Resolution|resolution]] 1.70Å' scene=''>
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| - | == Structural highlights ==
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| - | <table><tr><td colspan='2'>[[3brr]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3BRR OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3BRR FirstGlance]. <br>
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| - | </td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SLF:SULFATE-3-D-GALACTOSYL-BETA-1-1-N-STEAROYL-D-SPHINGOSINE'>SLF</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
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| - | <tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[1zni|1zni]]</td></tr>
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| - | <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 Homo sapiens])</td></tr>
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| - | <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=3brr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3brr OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3brr RCSB], [http://www.ebi.ac.uk/pdbsum/3brr PDBsum]</span></td></tr>
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| - | </table>
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| - | == 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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| - | == Evolutionary Conservation ==
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| - | [[Image:Consurf_key_small.gif|200px|right]]
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| - | Check<jmol>
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| - | <jmolCheckbox>
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| - | <scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/br/3brr_consurf.spt"</scriptWhenChecked>
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| - | <scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
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| - | <text>to colour the structure by Evolutionary Conservation</text>
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| - | </jmolCheckbox>
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| - | </jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/chain_selection.php?pdb_ID=2ata ConSurf].
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| - | <div style="clear:both"></div>
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| - | ==See Also==
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| - | *[[Molecular Playground/Insulin|Molecular Playground/Insulin]]
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| - | == References ==
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| - | <references/>
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| - | __TOC__
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| - | </StructureSection>
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| - | [[Category: Homo sapiens]]
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| - | [[Category: Bailey, K]]
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| - | [[Category: Buschard, K]]
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| - | [[Category: Hernandez-Prada, J A]]
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| - | [[Category: Magis, A T]]
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| - | [[Category: Ostrov, D A]]
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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: Secreted]]
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| - | [[Category: Sulfatide]]
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