View source for 2k91

{{STRUCTURE_2k91|  PDB=2k91  |  SCENE=  }} 
===Enhancing the activity of insulin by stereospecific unfolding===
{{ABSTRACT_PUBMED_19321436}}

==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. 

==About this Structure==
[[2k91]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2K91 OCA]. 

==See Also==
*[[Molecular Playground/Insulin|Molecular Playground/Insulin]]

==Reference==
<ref group="xtra">PMID:019321436</ref><references group="xtra"/><references/>
[[Category: Homo sapiens]]
[[Category: Hu, S Q.]]
[[Category: Hua, Q X.]]
[[Category: Huang, K.]]
[[Category: Jia, W H.]]
[[Category: Katsoyannis, P G.]]
[[Category: Nakarawa, S.]]
[[Category: Philips, N F.P.]]
[[Category: Weiss, M A.]]
[[Category: Wittaker, J.]]
[[Category: Wittaker, L.]]
[[Category: Xu, B.]]
[[Category: Carbohydrate metabolism]]
[[Category: Cleavage on pair of basic residue]]
[[Category: Diabetes mellitus]]
[[Category: Disease mutation]]
[[Category: Glucose metabolism]]
[[Category: Hormone]]
[[Category: Insulin]]
[[Category: Mutant]]
[[Category: Secreted]]