3p33: Difference between revisions

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{{STRUCTURE_3p33|  PDB=3p33  |  SCENE=  }}
===Insulin fibrillation is the Janus face of induced fit. A chiral clamp stabilizes the native state at the expense of activity===
{{ABSTRACT_PUBMED_15794638}}


==Disease==
==Insulin fibrillation is the Janus face of induced fit. A chiral clamp stabilizes the native state at the expense of activity==
[[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>  
<StructureSection load='3p33' size='340' side='right'caption='[[3p33]], [[Resolution|resolution]] 2.30&Aring;' scene=''>
 
== Structural highlights ==
==Function==
<table><tr><td colspan='2'>[[3p33]] 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=3P33 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3P33 FirstGlance]. <br>
[[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.
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.3&#8491;</td></tr>
 
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
==About this Structure==
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=3p33 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3p33 OCA], [https://pdbe.org/3p33 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3p33 RCSB], [https://www.ebi.ac.uk/pdbsum/3p33 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3p33 ProSAT]</span></td></tr>
[[3p33]] is a 8 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3P33 OCA].  
</table>
== Disease ==
[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>  
== Function ==
[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.


==See Also==
==See Also==
*[[Molecular Playground/Insulin|Molecular Playground/Insulin]]
*[[Insulin 3D Structures|Insulin 3D Structures]]
 
== References ==
==Reference==
<references/>
<ref group="xtra">PMID:015794638</ref><ref group="xtra">PMID:014596591</ref><ref group="xtra">PMID:015610006</ref><ref group="xtra">PMID:002905485</ref><ref group="xtra">PMID:002648161</ref><references group="xtra"/><references/>
__TOC__
[[Category: Dodson, G G.]]
</StructureSection>
[[Category: Hu, S Q.]]
[[Category: Homo sapiens]]
[[Category: Hua, Q X.]]
[[Category: Large Structures]]
[[Category: Huang, K.]]
[[Category: Dodson GG]]
[[Category: Jia, W H.]]
[[Category: Hu SQ]]
[[Category: Katsoyannis, P G.]]
[[Category: Hua QX]]
[[Category: Phillip, N F.]]
[[Category: Huang K]]
[[Category: Wan, Z L.]]
[[Category: Jia WH]]
[[Category: Weiss, M A.]]
[[Category: Katsoyannis PG]]
[[Category: Whittingham, J.]]
[[Category: Phillip NF]]
[[Category: Global health]]
[[Category: Wan ZL]]
[[Category: Hormone]]
[[Category: Weiss MA]]
[[Category: Insulin fibrillation]]
[[Category: Whittingham J]]
[[Category: Long-acting insulin analog]]
[[Category: Receptor binding protein engineering]]
[[Category: Zinc-binding site]]
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