5mwq

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'''Unreleased structure'''
 
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The entry 5mwq is ON HOLD until Paper Publication
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==Biosynthetic engineered A21K-B31K-B32R human insulin monomer structure in water/acetonitrile solution==
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<StructureSection load='5mwq' size='340' side='right' caption='[[5mwq]], [[NMR_Ensembles_of_Models | 20 NMR models]]' scene=''>
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Authors: Bocian, W., Kozerski, L.
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== Structural highlights ==
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<table><tr><td colspan='2'>[[5mwq]] is a 2 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5MWQ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5MWQ FirstGlance]. <br>
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Description: Biosynthetic engineered A21K-B31K-B32R human insulin monomer structure in water/acetonitrile solution
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</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=5mwq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5mwq OCA], [http://pdbe.org/5mwq PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5mwq RCSB], [http://www.ebi.ac.uk/pdbsum/5mwq PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5mwq ProSAT]</span></td></tr>
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[[Category: Unreleased Structures]]
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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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== References ==
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<references/>
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__TOC__
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</StructureSection>
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[[Category: Bocian, W]]
[[Category: Kozerski, L]]
[[Category: Kozerski, L]]
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[[Category: Bocian, W]]
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[[Category: Biosynthetic protein]]
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[[Category: Human insulin]]
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[[Category: Mutant]]
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[[Category: Water/acetonitrile solution]]

Revision as of 06:22, 15 February 2018

Biosynthetic engineered A21K-B31K-B32R human insulin monomer structure in water/acetonitrile solution

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