2mvc - Revision history

OCA at 18:57, 29 November 2023

OCA — Wed, 29 Nov 2023 18:57:00 GMT

←Older revision		Revision as of 18:57, 29 November 2023
Line 1:		Line 1:

	==Solution structure of human insulin at pH 1.9==		==Solution structure of human insulin at pH 1.9==
-	<StructureSection load='2mvc' size='340' side='right'caption='[[2mvc~~]], [[NMR_Ensembles_of_Models \| 50 NMR models~~]]' scene=''>	+	<StructureSection load='2mvc' size='340' side='right'caption='[[2mvc]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2mvc]] is a 2 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2MVC OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2MVC FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2mvc]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2MVC OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2MVC 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;'>[[2hiu\|2hiu]], [[2mvd\|2mvd]]</div~~></td></tr>	+	</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">Solution NMR</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=2mvc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2mvc OCA], [https://pdbe.org/2mvc PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2mvc RCSB], [https://www.ebi.ac.uk/pdbsum/2mvc PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2mvc 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=2mvc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2mvc OCA], [https://pdbe.org/2mvc PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2mvc RCSB], [https://www.ebi.ac.uk/pdbsum/2mvc PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2mvc 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.
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 27:		Line 27:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Brzozowski~~, A M~~]]	+	[[Category: Brzozowski AM]]
-	[[Category: Hexnerova, R]]	+	[[Category: Hexnerova R]]
-	[[Category: Jiracek, J]]	+	[[Category: Jiracek J]]
-	[[Category: Krizkova, K]]	+	[[Category: Krizkova K]]
-	[[Category: Maletinska, L]]	+	[[Category: Maletinska L]]
-	[[Category: Veverka, V]]	+	[[Category: Veverka V]]
-	[[Category: Zakova, L]]	+	[[Category: Zakova L]]
-	~~[[Category: Hormone]]~~	+
-	~~[[Category: Insulin~~]]	+

OCA at 09:03, 23 February 2022

OCA — Wed, 23 Feb 2022 09:03:33 GMT

←Older revision		Revision as of 09:03, 23 February 2022
Line 3:		Line 3:
	<StructureSection load='2mvc' size='340' side='right'caption='[[2mvc]], [[NMR_Ensembles_of_Models \| 50 NMR models]]' scene=''>		<StructureSection load='2mvc' size='340' side='right'caption='[[2mvc]], [[NMR_Ensembles_of_Models \| 50 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2mvc]] is a 2 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2MVC OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://proteopedia.org/fgij/fg.htm?mol=2MVC FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2mvc]] is a 2 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2MVC OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2MVC FirstGlance]. <br>
-	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2hiu\|2hiu]], [[2mvd\|2mvd]]</td></tr>	+	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[2hiu\|2hiu]], [[2mvd\|2mvd]]</div></td></tr>
-	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://proteopedia.org/fgij/fg.htm?mol=2mvc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2mvc OCA], [~~http~~://pdbe.org/2mvc PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=2mvc RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/2mvc PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=2mvc 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=2mvc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2mvc OCA], [https://pdbe.org/2mvc PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2mvc RCSB], [https://www.ebi.ac.uk/pdbsum/2mvc PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2mvc ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== 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>	+	[[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 ==
-	[[~~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.	+	[[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.
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==

OCA at 06:28, 20 May 2020

OCA — Wed, 20 May 2020 06:28:51 GMT

←Older revision		Revision as of 06:28, 20 May 2020
Line 1:		Line 1:

	==Solution structure of human insulin at pH 1.9==		==Solution structure of human insulin at pH 1.9==
-	<StructureSection load='2mvc' size='340' side='right' caption='[[2mvc]], [[NMR_Ensembles_of_Models \| 50 NMR models]]' scene=''>	+	<StructureSection load='2mvc' size='340' side='right'caption='[[2mvc]], [[NMR_Ensembles_of_Models \| 50 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2mvc]] is a 2 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2MVC OCA]. For a <b>guided tour on the structure components</b> use [http://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=2MVC FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2mvc]] is a 2 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2MVC OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=2MVC FirstGlance]. <br>
	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2hiu\|2hiu]], [[2mvd\|2mvd]]</td></tr>		</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2hiu\|2hiu]], [[2mvd\|2mvd]]</td></tr>
-	<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=2mvc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2mvc OCA], [http://pdbe.org/2mvc PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2mvc RCSB], [http://www.ebi.ac.uk/pdbsum/2mvc PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2mvc ProSAT]</span></td></tr>	+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://proteopedia.org/fgij/fg.htm?mol=2mvc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2mvc OCA], [http://pdbe.org/2mvc PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2mvc RCSB], [http://www.ebi.ac.uk/pdbsum/2mvc PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2mvc ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 22:		Line 22:

	==See Also==		==See Also==
-	*[[~~Molecular Playground/~~Insulin\|~~Molecular Playground/~~Insulin]]	+	*[[Insulin 3D Structures\|Insulin 3D Structures]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Large Structures]]
	[[Category: Brzozowski, A M]]		[[Category: Brzozowski, A M]]
	[[Category: Hexnerova, R]]		[[Category: Hexnerova, R]]

OCA at 17:01, 15 August 2018

OCA — Wed, 15 Aug 2018 17:01:07 GMT

←Older revision		Revision as of 17:01, 15 August 2018
Line 5:		Line 5:
	<table><tr><td colspan='2'>[[2mvc]] is a 2 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2MVC OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2MVC FirstGlance]. <br>		<table><tr><td colspan='2'>[[2mvc]] is a 2 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2MVC OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2MVC FirstGlance]. <br>
	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2hiu\|2hiu]], [[2mvd\|2mvd]]</td></tr>		</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2hiu\|2hiu]], [[2mvd\|2mvd]]</td></tr>
-	<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=2mvc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2mvc OCA], [http://pdbe.org/2mvc PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2mvc RCSB], [http://www.ebi.ac.uk/pdbsum/2mvc PDBsum]</span></td></tr>	+	<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=2mvc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2mvc OCA], [http://pdbe.org/2mvc PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2mvc RCSB], [http://www.ebi.ac.uk/pdbsum/2mvc PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2mvc ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==

OCA at 07:47, 1 June 2016

OCA — Wed, 01 Jun 2016 07:47:15 GMT

←Older revision		Revision as of 07:47, 1 June 2016
Line 1:		Line 1:
		+
	==Solution structure of human insulin at pH 1.9==		==Solution structure of human insulin at pH 1.9==
	<StructureSection load='2mvc' size='340' side='right' caption='[[2mvc]], [[NMR_Ensembles_of_Models \| 50 NMR models]]' scene=''>		<StructureSection load='2mvc' size='340' side='right' caption='[[2mvc]], [[NMR_Ensembles_of_Models \| 50 NMR models]]' scene=''>

OCA at 09:08, 11 September 2015

OCA — Fri, 11 Sep 2015 09:08:46 GMT

←Older revision		Revision as of 09:08, 11 September 2015
Line 4:		Line 4:
	<table><tr><td colspan='2'>[[2mvc]] is a 2 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2MVC OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2MVC FirstGlance]. <br>		<table><tr><td colspan='2'>[[2mvc]] is a 2 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2MVC OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2MVC FirstGlance]. <br>
	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2hiu\|2hiu]], [[2mvd\|2mvd]]</td></tr>		</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2hiu\|2hiu]], [[2mvd\|2mvd]]</td></tr>
-	<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=2mvc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2mvc OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2mvc RCSB], [http://www.ebi.ac.uk/pdbsum/2mvc PDBsum]</span></td></tr>	+	<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=2mvc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2mvc OCA], [http://pdbe.org/2mvc PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2mvc RCSB], [http://www.ebi.ac.uk/pdbsum/2mvc PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 18:		Line 18:
	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>		From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
	</div>		</div>
		+	<div class="pdbe-citations 2mvc" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 16:09, 10 December 2014

OCA — Wed, 10 Dec 2014 16:09:34 GMT

←Older revision		Revision as of 16:09, 10 December 2014
Line 1:		Line 1:
-	'''~~Unreleased~~ structure'''	+	==Solution structure of human insulin at pH 1.9==
		+	<StructureSection load='2mvc' size='340' side='right' caption='[[2mvc]], [[NMR_Ensembles_of_Models \| 50 NMR models]]' scene=''>
		+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[2mvc]] is a 2 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2MVC OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2MVC FirstGlance]. <br>
		+	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[2hiu\|2hiu]], [[2mvd\|2mvd]]</td></tr>
		+	<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=2mvc FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2mvc OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2mvc RCSB], [http://www.ebi.ac.uk/pdbsum/2mvc 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.
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	The insulin gene mutation c.137G>A (R46Q), which changes an arginine at the B22 position of the mature hormone to glutamine, causes the monogenic diabetes variant maturity-onset diabetes of the young (MODY). In MODY patients, this mutation is heterozygous, and both mutant and wild-type (WT) human insulin are produced simultaneously. However, the patients often depend on administration of exogenous insulin. In this study, we chemically synthesized the MODY mutant [GlnB22]-insulin and characterized its biological and structural properties. The chemical synthesis of this insulin analogue revealed that its folding ability is severely impaired. In vitro and in vivo tests showed that its binding affinity and biological activity are reduced (both approximately 20% that of human insulin). Comparison of the solution structure of [GlnB22]-insulin with the solution structure of native human insulin revealed that the most significant structural effect of the mutation is distortion of the B20-B23 beta-turn, leading to liberation of the B chain C-terminus from the protein core. The distortion of the B20-B23 beta-turn is caused by the extended conformational freedom of the GlnB22 side chain, which is no longer anchored in a hydrogen bonding network like the native ArgB22. The partially disordered [GlnB22]-insulin structure appears to be one reason for the reduced binding potency of this mutant and may also be responsible for its low folding efficiency in vivo. The altered orientation and flexibility of the B20-B23 beta-turn may interfere with the formation of disulfide bonds in proinsulin bearing the R46Q (GlnB22) mutation. This may also have a negative effect on the WT proinsulin simultaneously biosynthesized in beta-cells and therefore play a major role in the development of MODY in patients producing [GlnB22]-insulin.

-	~~The entry 2mvc is ON HOLD until Paper Publication~~	+	Structural and Functional Study of the GlnB22-Insulin Mutant Responsible for Maturity-Onset Diabetes of the Young.,Krizkova K, Veverka V, Maletinska L, Hexnerova R, Brzozowski AM, Jiracek J, Zakova L PLoS One. 2014 Nov 25;9(11):e112883. doi: 10.1371/journal.pone.0112883., eCollection 2014. PMID:25423173<ref>PMID:25423173</ref>

-	~~Authors~~: Hexnerova, R., Krizkova, K., Maletinska, L~~., Jiracek, J., Brzozowski, A.M.~~, Zakova, L~~., Veverka, V.~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-		+	</div>
-	~~Description~~: ~~Solution structure of human insulin at pH 1.9~~	+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Brzozowski, A M]]
		+	[[Category: Hexnerova, R]]
		+	[[Category: Jiracek, J]]
		+	[[Category: Krizkova, K]]
		+	[[Category: Maletinska, L]]
		+	[[Category: Veverka, V]]
		+	[[Category: Zakova, L]]
		+	[[Category: Hormone]]
		+	[[Category: Insulin]]

OCA at 10:59, 19 November 2014

OCA — Wed, 19 Nov 2014 10:59:33 GMT

←Older revision		Revision as of 10:59, 19 November 2014
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	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 2mvc is ON HOLD	+	The entry 2mvc is ON HOLD until Paper Publication

	Authors: Hexnerova, R., Krizkova, K., Maletinska, L., Jiracek, J., Brzozowski, A.M., Zakova, L., Veverka, V.		Authors: Hexnerova, R., Krizkova, K., Maletinska, L., Jiracek, J., Brzozowski, A.M., Zakova, L., Veverka, V.

	Description: Solution structure of human insulin at pH 1.9		Description: Solution structure of human insulin at pH 1.9

OCA: Protected "2mvc" [edit=sysop:move=sysop]

OCA — Sun, 12 Oct 2014 13:48:14 GMT

Protected "2mvc" [edit=sysop:move=sysop]

←Older revision

Revision as of 13:48, 12 October 2014

OCA: New page: '''Unreleased structure''' The entry 2mvc is ON HOLD Authors: Hexnerova, R., Krizkova, K., Maletinska, L., Jiracek, J., Brzozowski, A.M., Zakova, L., Veverka, V. Description: Solution ...

OCA — Sun, 12 Oct 2014 13:48:13 GMT

New page: '''Unreleased structure''' The entry 2mvc is ON HOLD Authors: Hexnerova, R., Krizkova, K., Maletinska, L., Jiracek, J., Brzozowski, A.M., Zakova, L., Veverka, V. Description: Solution ...

New page

'''Unreleased structure'''

The entry 2mvc is ON HOLD

Authors: Hexnerova, R., Krizkova, K., Maletinska, L., Jiracek, J., Brzozowski, A.M., Zakova, L., Veverka, V.

Description: Solution structure of human insulin at pH 1.9