2c8q: Difference between revisions

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== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[2c8q]] is a 2 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=2C8Q OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2C8Q FirstGlance]. <br>
<table><tr><td colspan='2'>[[2c8q]] is a 2 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=2C8Q OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2C8Q FirstGlance]. <br>
</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[1a7f|1a7f]], [[1ai0|1ai0]], [[1aiy|1aiy]], [[1b9e|1b9e]], [[1ben|1ben]], [[1efe|1efe]], [[1ev3|1ev3]], [[1ev6|1ev6]], [[1evr|1evr]], [[1fu2|1fu2]], [[1fub|1fub]], [[1g7a|1g7a]], [[1g7b|1g7b]], [[1guj|1guj]], [[1hiq|1hiq]], [[1his|1his]], [[1hit|1hit]], [[1hls|1hls]], [[1htv|1htv]], [[1hui|1hui]], [[1iog|1iog]], [[1ioh|1ioh]], [[1j73|1j73]], [[1jca|1jca]], [[1jco|1jco]], [[1k3m|1k3m]], [[1kmf|1kmf]], [[1lkq|1lkq]], [[1lnp|1lnp]], [[1lph|1lph]], [[1mhi|1mhi]], [[1mhj|1mhj]], [[1mso|1mso]], [[1os3|1os3]], [[1os4|1os4]], [[1q4v|1q4v]], [[1qiy|1qiy]], [[1qiz|1qiz]], [[1qj0|1qj0]], [[1rwe|1rwe]], [[1sf1|1sf1]], [[1sjt|1sjt]], [[1sju|1sju]], [[1t0c|1t0c]], [[1t1k|1t1k]], [[1t1p|1t1p]], [[1t1q|1t1q]], [[1trz|1trz]], [[1tyl|1tyl]], [[1tym|1tym]], [[1uz9|1uz9]], [[1vkt|1vkt]], [[1w8p|1w8p]], [[1xda|1xda]], [[1xgl|1xgl]], [[1xw7|1xw7]], [[1zeg|1zeg]], [[1zeh|1zeh]], [[1znj|1znj]], [[2c8r|2c8r]], [[2aiy|2aiy]], [[2hiu|2hiu]], [[3aiy|3aiy]], [[4aiy|4aiy]], [[5aiy|5aiy]]</div></td></tr>
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.95&#8491;</td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=2c8q FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2c8q OCA], [https://pdbe.org/2c8q PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2c8q RCSB], [https://www.ebi.ac.uk/pdbsum/2c8q PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2c8q ProSAT]</span></td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=2c8q FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2c8q OCA], [https://pdbe.org/2c8q PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2c8q RCSB], [https://www.ebi.ac.uk/pdbsum/2c8q PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2c8q ProSAT]</span></td></tr>
</table>
</table>
== Disease ==
== 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>
[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 ==
== 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.  
[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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== Publication Abstract from PubMed ==
== Publication Abstract from PubMed ==
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[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Large Structures]]
[[Category: Large Structures]]
[[Category: Bourgeois, D]]
[[Category: Bourgeois D]]
[[Category: Cipriani, F]]
[[Category: Cipriani F]]
[[Category: Felisaz, F]]
[[Category: Felisaz F]]
[[Category: Jacquamet, L]]
[[Category: Jacquamet L]]
[[Category: Joly, J]]
[[Category: Joly J]]
[[Category: Lavault, B]]
[[Category: Lavault B]]
[[Category: Nurizzo, D]]
[[Category: Nurizzo D]]
[[Category: Ohana, J]]
[[Category: Ohana J]]
[[Category: Vernede, X]]
[[Category: Vernede X]]
[[Category: Carbohydrate metabolism]]
[[Category: Diabetes mellitus]]
[[Category: Glucose metabolism]]
[[Category: Hormone]]
[[Category: Laser]]
[[Category: Uv]]

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