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1g7a

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[[Image:1g7a.png|left|200px]]
 
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==1.2 A structure of T3R3 human insulin at 100 K==
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The line below this paragraph, containing "STRUCTURE_1g7a", creates the "Structure Box" on the page.
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<StructureSection load='1g7a' size='340' side='right'caption='[[1g7a]], [[Resolution|resolution]] 1.20&Aring;' scene=''>
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You may change the PDB parameter (which sets the PDB file loaded into the applet)
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== Structural highlights ==
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or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
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<table><tr><td colspan='2'>[[1g7a]] is a 8 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=1G7A OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1G7A FirstGlance]. <br>
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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]] 1.2&#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=ACN:ACETONE'>ACN</scene>, <scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
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{{STRUCTURE_1g7a| PDB=1g7a | SCENE= }}
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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=1g7a FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1g7a OCA], [https://pdbe.org/1g7a PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1g7a RCSB], [https://www.ebi.ac.uk/pdbsum/1g7a PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1g7a ProSAT]</span></td></tr>
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</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.
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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/g7/1g7a_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=1g7a ConSurf].
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<div style="clear:both"></div>
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<div style="background-color:#fffaf0;">
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== Publication Abstract from PubMed ==
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The structure of T(3)R(3) hexameric human insulin has been determined at 100 K from two different crystals at 1.2 and 1.3 A resolution and refined to residuals of 0.169 and 0.176, respectively. Owing to a phase change, the c axis is double its room-temperature value and the asymmetric unit contains two independent TR(f) insulin dimers. Compared with the orientation in the room-temperature structure, one dimer undergoes a rotation about the c axis of -5 degrees, while the second is rotated +4 degrees. A superposition of the backbone atoms of the two independent dimers shows that the C(alpha) atoms of five residues within the R(f)-state monomers are displaced by more than 1.0 A; smaller displacements are observed for the T-state monomers. Four zinc ions lie on the crystallographic threefold axis and each forms bonds to three symmetry-related HisB10 N(varepsilon2) atoms from the T- and R(f)-state trimers. While three of the zinc ions are tetrahedrally coordinated with a chloride ion completing the coordination sphere, mixed tetrahedral/octahedral coordination is observed for one of the T-state zinc ions. The three symmetry-related "phenolic binding sites" in one hexamer contain water molecules and a glycerol molecule, but the same sites in the second hexamer are occupied by a zinc ion coordinated to an alternate conformation of HisB10, a symmetry-related HisB5 and two chloride ions. Two additional and partially occupied zinc ion sites are observed at the interface between the two independent dimers. One zinc ion is coordinated by a T-state HisB5 of one dimer, an R-state HisB5 of the second dimer and two water molecules; the second zinc ion is coordinated by an alternate side-chain conformation of the T-state HisB5 and three water molecules. The carboxyl group of one GluB13 side chain, which exists in two discrete conformations, appears to be protonated, because short contacts exist to a second carboxyl group or to a carbonyl O atom.
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===1.2 A structure of T3R3 human insulin at 100 K===
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Phase changes in T(3)R(3)(f) human insulin: temperature or pressure induced?,Smith GD, Pangborn WA, Blessing RH Acta Crystallogr D Biol Crystallogr. 2001 Aug;57(Pt 8):1091-100. Epub 2001, Jul 23. PMID:11468392<ref>PMID:11468392</ref>
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From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
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The line below this paragraph, {{ABSTRACT_PUBMED_11468392}}, adds the Publication Abstract to the page
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<div class="pdbe-citations 1g7a" style="background-color:#fffaf0;"></div>
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(as it appears on PubMed at http://www.pubmed.gov), where 11468392 is the PubMed ID number.
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{{ABSTRACT_PUBMED_11468392}}
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==About this Structure==
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[[1g7a]] is a 8 chain structure of [[Molecular Playground/Insulin]]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1G7A OCA].
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==See Also==
==See Also==
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*[[Molecular Playground/Insulin]]
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*[[Insulin 3D Structures|Insulin 3D Structures]]
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== References ==
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==Reference==
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<references/>
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<ref group="xtra">PMID:011468392</ref><references group="xtra"/>
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__TOC__
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[[Category: Blessing, R H.]]
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</StructureSection>
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[[Category: Pangborn, W A.]]
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[[Category: Homo sapiens]]
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[[Category: Smith, G D.]]
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[[Category: Large Structures]]
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[[Category: Hormone-growth factor complex]]
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[[Category: Blessing RH]]
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[[Category: T3r3 insulin hexamer]]
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[[Category: Pangborn WA]]
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[[Category: Smith GD]]

Current revision

1.2 A structure of T3R3 human insulin at 100 K

PDB ID 1g7a

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