OCA at 10:02, 20 December 2023

2023-12-20T10:02:11Z

←Older revision		Revision as of 10:02, 20 December 2023
Line 1:		Line 1:
-	'''Unreleased structure'''

-	~~The entry~~ 8hsk is ~~ON HOLD until Paper Publication~~	+	==Insulin single mutant INS-Q==
-		+	<StructureSection load='8hsk' size='340' side='right'caption='[[8hsk]], [[Resolution\|resolution]] 1.64Å' scene=''>
-	~~Authors~~: ~~Rao~~, S.S., ~~Kundapura~~, S.V., ~~Kulal~~, A., ~~Ramagopal~~, U.A.	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[8hsk]] 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=8HSK OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8HSK FirstGlance]. <br>
-	~~Description~~: Insulin ~~single mutant INS-Q~~	+	</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution\|Resolution]] 1.64Å</td></tr>
-	[[Category: ~~Unreleased Structures~~]]	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
-	[[Category: ~~Rao, S.S~~]]	+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=8hsk FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8hsk OCA], [https://pdbe.org/8hsk PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8hsk RCSB], [https://www.ebi.ac.uk/pdbsum/8hsk PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8hsk ProSAT]</span></td></tr>
-	[[Category: ~~Ramagopal, U.~~A]]	+	</table>
-	[[Category: ~~Kulal, A~~]]	+	== Disease ==
-	[[Category: ~~Kundapura, S.V~~]]	+	[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.
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Homo sapiens]]
		+	[[Category: Large Structures]]
		+	[[Category: Kulal A]]
		+	[[Category: Kundapura SV]]
		+	[[Category: Ramagopal UA]]
		+	[[Category: Rao SS]]

OCA at 05:22, 8 February 2023

2023-02-08T05:22:25Z

←Older revision		Revision as of 05:22, 8 February 2023
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 8hsk is ON HOLD	+	The entry 8hsk is ON HOLD until Paper Publication

	Authors: Rao, S.S., Kundapura, S.V., Kulal, A., Ramagopal, U.A.		Authors: Rao, S.S., Kundapura, S.V., Kulal, A., Ramagopal, U.A.

OCA: Protected "8hsk" [edit=sysop:move=sysop]

2022-12-28T06:29:15Z

Protected "8hsk" [edit=sysop:move=sysop]

←Older revision

Revision as of 06:29, 28 December 2022

OCA: New page: '''Unreleased structure''' The entry 8hsk is ON HOLD Authors: Rao, S.S., Kundapura, S.V., Kulal, A., Ramagopal, U.A. Description: Insulin single mutant INS-Q [[Category: Unreleased Str...

2022-12-28T06:29:12Z

New page: '''Unreleased structure''' The entry 8hsk is ON HOLD Authors: Rao, S.S., Kundapura, S.V., Kulal, A., Ramagopal, U.A. Description: Insulin single mutant INS-Q [[Category: Unreleased Str...

New page

'''Unreleased structure'''

The entry 8hsk is ON HOLD

Authors: Rao, S.S., Kundapura, S.V., Kulal, A., Ramagopal, U.A.

Description: Insulin single mutant INS-Q
[[Category: Unreleased Structures]]
[[Category: Rao, S.S]]
[[Category: Ramagopal, U.A]]
[[Category: Kulal, A]]
[[Category: Kundapura, S.V]]

8hsk - Revision history

OCA at 10:02, 20 December 2023

OCA at 05:22, 8 February 2023

OCA: Protected "8hsk" [edit=sysop:move=sysop]

OCA: New page: '''Unreleased structure''' The entry 8hsk is ON HOLD Authors: Rao, S.S., Kundapura, S.V., Kulal, A., Ramagopal, U.A. Description: Insulin single mutant INS-Q [[Category: Unreleased Str...