3v19: Difference between revisions
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==Forestalling insulin fibrillation by insertion of a chiral clamp mechanism-based application of protein engineering to global health== | |||
<StructureSection load='3v19' size='340' side='right' caption='[[3v19]], [[Resolution|resolution]] 2.00Å' scene=''> | |||
== Structural highlights == | |||
==Disease== | <table><tr><td colspan='2'>[[3v19]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3V19 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3V19 FirstGlance]. <br> | ||
[[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> | </td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><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> | ||
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[3v1g|3v1g]]</td></tr> | |||
==Function== | <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=3v19 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3v19 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3v19 RCSB], [http://www.ebi.ac.uk/pdbsum/3v19 PDBsum]</span></td></tr> | ||
</table> | |||
== Disease == | |||
[[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> | |||
== Function == | |||
[[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. | [[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. | ||
==See Also== | ==See Also== | ||
*[[Molecular Playground/Insulin|Molecular Playground/Insulin]] | *[[Molecular Playground/Insulin|Molecular Playground/Insulin]] | ||
== References == | |||
== | <references/> | ||
<references | __TOC__ | ||
[[Category: Hu, S Q | </StructureSection> | ||
[[Category: Hua, Q X | [[Category: Hu, S Q]] | ||
[[Category: Huang, K | [[Category: Hua, Q X]] | ||
[[Category: Ismail-Beigi, F | [[Category: Huang, K]] | ||
[[Category: Katsoyyannis, P G | [[Category: Ismail-Beigi, F]] | ||
[[Category: Petkova, A T | [[Category: Katsoyyannis, P G]] | ||
[[Category: Phillips, N B | [[Category: Petkova, A T]] | ||
[[Category: Tycko, R | [[Category: Phillips, N B]] | ||
[[Category: Wan, Z L | [[Category: Tycko, R]] | ||
[[Category: Weiss, M A | [[Category: Wan, Z L]] | ||
[[Category: Whittake, J | [[Category: Weiss, M A]] | ||
[[Category: Wickramasinghe, N P | [[Category: Whittake, J]] | ||
[[Category: Yeh, I J | [[Category: Wickramasinghe, N P]] | ||
[[Category: Yeh, I J]] | |||
[[Category: Hormone]] | [[Category: Hormone]] | ||
[[Category: Insulin fibrillation]] | [[Category: Insulin fibrillation]] | ||
