|
|
| (2 intermediate revisions not shown.) |
| Line 1: |
Line 1: |
| - | {{STRUCTURE_3brr| PDB=3brr | SCENE= }}
| + | #REDIRECT [[4xc4]] This PDB entry is obsolete and replaced by 4xc4 |
| - | ===Crystal Structure of Insulin in Complex with Sulfatide===
| + | |
| - | | + | |
| - | ==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==
| + | |
| - | [[3brr]] 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=3BRR OCA].
| + | |
| - | | + | |
| - | ==See Also==
| + | |
| - | *[[Molecular Playground/Insulin|Molecular Playground/Insulin]]
| + | |
| - | | + | |
| - | ==Reference==
| + | |
| - | <references group="xtra"/><references/>
| + | |
| - | [[Category: Homo sapiens]]
| + | |
| - | [[Category: Bailey, K.]]
| + | |
| - | [[Category: Buschard, K.]]
| + | |
| - | [[Category: Hernandez-Prada, J A.]]
| + | |
| - | [[Category: Magis, A T.]]
| + | |
| - | [[Category: Ostrov, D A.]]
| + | |
| - | [[Category: Carbohydrate metabolism]]
| + | |
| - | [[Category: Cleavage on pair of basic residue]]
| + | |
| - | [[Category: Diabetes mellitus]]
| + | |
| - | [[Category: Disease mutation]]
| + | |
| - | [[Category: Glucose metabolism]]
| + | |
| - | [[Category: Hormone]]
| + | |
| - | [[Category: Insulin]]
| + | |
| - | [[Category: Secreted]]
| + | |
| - | [[Category: Sulfatide]]
| + | |
