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2g54

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{{STRUCTURE_2g54| PDB=2g54 | SCENE= }}
 
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===Crystal structure of Zn-bound human insulin-degrading enzyme in complex with insulin B chain===
 
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{{ABSTRACT_PUBMED_17051221}}
 
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==Disease==
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==Crystal structure of Zn-bound human insulin-degrading enzyme in complex with insulin B chain==
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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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<StructureSection load='2g54' size='340' side='right'caption='[[2g54]], [[Resolution|resolution]] 2.25&Aring;' scene=''>
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== Structural highlights ==
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==Function==
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<table><tr><td colspan='2'>[[2g54]] is a 4 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2G54 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2G54 FirstGlance]. <br>
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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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</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.25&#8491;</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=DIO:1,4-DIETHYLENE+DIOXIDE'>DIO</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
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==About this Structure==
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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=2g54 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2g54 OCA], [https://pdbe.org/2g54 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2g54 RCSB], [https://www.ebi.ac.uk/pdbsum/2g54 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2g54 ProSAT]</span></td></tr>
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[[2g54]] 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=2G54 OCA].
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</table>
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== Function ==
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[https://www.uniprot.org/uniprot/IDE_HUMAN IDE_HUMAN] Plays a role in the cellular breakdown of insulin, IAPP, glucagon, bradykinin, kallidin and other peptides, and thereby plays a role in intercellular peptide signaling. Degrades amyloid formed by APP and IAPP. May play a role in the degradation and clearance of naturally secreted amyloid beta-protein by neurons and microglia.<ref>PMID:10684867</ref> <ref>PMID:17613531</ref> <ref>PMID:18986166</ref>
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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/g5/2g54_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/main_output.php?pdb_ID=2g54 ConSurf].
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<div style="clear:both"></div>
==See Also==
==See Also==
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*[[Insulin 3D Structures|Insulin 3D Structures]]
*[[Insulin-Degrading Enzyme|Insulin-Degrading Enzyme]]
*[[Insulin-Degrading Enzyme|Insulin-Degrading Enzyme]]
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*[[Journal:JBSD:29|Journal:JBSD:29]]
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*[[Insulin-degrading enzyme 3D structures|Insulin-degrading enzyme 3D structures]]
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*[[Molecular Playground/Insulin|Molecular Playground/Insulin]]
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== References ==
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<references/>
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==Reference==
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__TOC__
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<ref group="xtra">PMID:017051221</ref><ref group="xtra">doi 10.1080/07391102.2012.732340</ref><references group="xtra"/><references/>
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</StructureSection>
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
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[[Category: Insulysin]]
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[[Category: Large Structures]]
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[[Category: Shen, Y.]]
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[[Category: Shen Y]]
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[[Category: Tang, W J.]]
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[[Category: Tang W-J]]
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[[Category: Hydrolase]]
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[[Category: Protein-peptide complex]]
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Current revision

Crystal structure of Zn-bound human insulin-degrading enzyme in complex with insulin B chain

PDB ID 2g54

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