2l1z - Revision history

OCA at 10:36, 16 August 2023

OCA — Wed, 16 Aug 2023 10:36:03 GMT

←Older revision		Revision as of 10:36, 16 August 2023
Line 1:		Line 1:

	==NMR Structure of human insulin mutant GLY-B20-D-ALA, GLY-B23-D-ALA PRO-B28-LYS, LYS-B29-PRO, 20 Structures==		==NMR Structure of human insulin mutant GLY-B20-D-ALA, GLY-B23-D-ALA PRO-B28-LYS, LYS-B29-PRO, 20 Structures==
-	<StructureSection load='2l1z' size='340' side='right'caption='[[2l1z~~]], [[NMR_Ensembles_of_Models \| 20 NMR models~~]]' scene=''>	+	<StructureSection load='2l1z' size='340' side='right'caption='[[2l1z]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2l1z]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/~~Human Human~~]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2L1Z OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2L1Z FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2l1z]] 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=2L1Z OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2L1Z 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;'>[[3oal\|3oal]], [[3ob3\|3ob3]], [[3ob5\|3ob5]], [[2l1y\|2l1y]]</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~~='gene'><td class~~="~~sblockLbl~~">~~<b>[[Gene\|Gene:]]</b></td><td class="sblockDat">INS ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])~~</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=2l1z FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2l1z OCA], [https://pdbe.org/2l1z PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2l1z RCSB], [https://www.ebi.ac.uk/pdbsum/2l1z PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2l1z 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=2l1z FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2l1z OCA], [https://pdbe.org/2l1z PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2l1z RCSB], [https://www.ebi.ac.uk/pdbsum/2l1z PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2l1z 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.

	==See Also==		==See Also==
Line 19:		Line 18:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Hu~~, S Q~~]]	+	[[Category: Hu SQ]]
-	[[Category: Hua~~, Q X~~]]	+	[[Category: Hua QX]]
-	[[Category: Huang, K]]	+	[[Category: Huang K]]
-	[[Category: Katsoyannis~~, J W~~]]	+	[[Category: Katsoyannis JW]]
-	[[Category: Philips~~, N B~~]]	+	[[Category: Philips NB]]
-	[[Category: Wan~~, Z L~~]]	+	[[Category: Wan ZL]]
-	[[Category: Weiss~~, M A]]~~	+	[[Category: Weiss MA]]
-	~~[[Category: Hormone]]~~	+
-	~~[[Category: Human insulin]]~~	+
-	~~[[Category: Mutant~~]]	+

OCA at 08:32, 10 November 2021

OCA — Wed, 10 Nov 2021 08:32:35 GMT

←Older revision		Revision as of 08:32, 10 November 2021
Line 3:		Line 3:
	<StructureSection load='2l1z' size='340' side='right'caption='[[2l1z]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>		<StructureSection load='2l1z' size='340' side='right'caption='[[2l1z]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2l1z]] is a 2 chain structure with sequence from [~~http~~://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2L1Z OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=2L1Z FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2l1z]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2L1Z OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2L1Z FirstGlance]. <br>
-	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3oal\|3oal]], [[3ob3\|3ob3]], [[3ob5\|3ob5]], [[2l1y\|2l1y]]</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;'>[[3oal\|3oal]], [[3ob3\|3ob3]], [[3ob5\|3ob5]], [[2l1y\|2l1y]]</div></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">INS ([~~http~~://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">INS ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=2l1z FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2l1z OCA], [~~http~~://pdbe.org/2l1z PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=2l1z RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/2l1z PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=2l1z 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=2l1z FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2l1z OCA], [https://pdbe.org/2l1z PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2l1z RCSB], [https://www.ebi.ac.uk/pdbsum/2l1z PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2l1z 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.

	==See Also==		==See Also==

OCA at 08:31, 5 February 2020

OCA — Wed, 05 Feb 2020 08:31:33 GMT

←Older revision		Revision as of 08:31, 5 February 2020
Line 1:		Line 1:

	==NMR Structure of human insulin mutant GLY-B20-D-ALA, GLY-B23-D-ALA PRO-B28-LYS, LYS-B29-PRO, 20 Structures==		==NMR Structure of human insulin mutant GLY-B20-D-ALA, GLY-B23-D-ALA PRO-B28-LYS, LYS-B29-PRO, 20 Structures==
-	<StructureSection load='2l1z' size='340' side='right' caption='[[2l1z]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>	+	<StructureSection load='2l1z' size='340' side='right'caption='[[2l1z]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2l1z]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2L1Z OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2L1Z FirstGlance]. <br>		<table><tr><td colspan='2'>[[2l1z]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2L1Z OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2L1Z FirstGlance]. <br>
Line 14:		Line 14:

	==See Also==		==See Also==
-	*[[~~Molecular Playground/~~Insulin\|~~Molecular Playground/~~Insulin]]	+	*[[Insulin 3D Structures\|Insulin 3D Structures]]
	== References ==		== References ==
	<references/>		<references/>
Line 20:		Line 20:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Hu, S Q]]		[[Category: Hu, S Q]]
	[[Category: Hua, Q X]]		[[Category: Hua, Q X]]

OCA at 08:11, 25 July 2018

OCA — Wed, 25 Jul 2018 08:11:04 GMT

←Older revision		Revision as of 08:11, 25 July 2018
Line 1:		Line 1:
		+
	==NMR Structure of human insulin mutant GLY-B20-D-ALA, GLY-B23-D-ALA PRO-B28-LYS, LYS-B29-PRO, 20 Structures==		==NMR Structure of human insulin mutant GLY-B20-D-ALA, GLY-B23-D-ALA PRO-B28-LYS, LYS-B29-PRO, 20 Structures==
	<StructureSection load='2l1z' size='340' side='right' caption='[[2l1z]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>		<StructureSection load='2l1z' size='340' side='right' caption='[[2l1z]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>
Line 5:		Line 6:
	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3oal\|3oal]], [[3ob3\|3ob3]], [[3ob5\|3ob5]], [[2l1y\|2l1y]]</td></tr>		</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3oal\|3oal]], [[3ob3\|3ob3]], [[3ob5\|3ob5]], [[2l1y\|2l1y]]</td></tr>
	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">INS ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>		<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">INS ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=2l1z FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2l1z OCA], [http://pdbe.org/2l1z PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2l1z RCSB], [http://www.ebi.ac.uk/pdbsum/2l1z 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=2l1z FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2l1z OCA], [http://pdbe.org/2l1z PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2l1z RCSB], [http://www.ebi.ac.uk/pdbsum/2l1z PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2l1z ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==

OCA at 04:03, 11 September 2015

OCA — Fri, 11 Sep 2015 04:03:36 GMT

←Older revision		Revision as of 04:03, 11 September 2015
Line 2:		Line 2:
	<StructureSection load='2l1z' size='340' side='right' caption='[[2l1z]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>		<StructureSection load='2l1z' size='340' side='right' caption='[[2l1z]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2l1z]] 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=2L1Z OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2L1Z FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2l1z]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2L1Z OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2L1Z FirstGlance]. <br>
	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3oal\|3oal]], [[3ob3\|3ob3]], [[3ob5\|3ob5]], [[2l1y\|2l1y]]</td></tr>		</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3oal\|3oal]], [[3ob3\|3ob3]], [[3ob5\|3ob5]], [[2l1y\|2l1y]]</td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">INS ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">INS ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=2l1z FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2l1z OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2l1z RCSB], [http://www.ebi.ac.uk/pdbsum/2l1z 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=2l1z FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2l1z OCA], [http://pdbe.org/2l1z PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2l1z RCSB], [http://www.ebi.ac.uk/pdbsum/2l1z PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 18:		Line 18:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Hu, S Q]]		[[Category: Hu, S Q]]
	[[Category: Hua, Q X]]		[[Category: Hua, Q X]]

OCA at 12:12, 18 December 2014

OCA — Thu, 18 Dec 2014 12:12:53 GMT

←Older revision		Revision as of 12:12, 18 December 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_2l1z\| PDB=2l1z \| SCENE= }}~~	+	==NMR Structure of human insulin mutant GLY-B20-D-ALA, GLY-B23-D-ALA PRO-B28-LYS, LYS-B29-PRO, 20 Structures==
-	===NMR Structure of human insulin mutant GLY-B20-D-ALA, GLY-B23-D-ALA PRO-B28-LYS, LYS-B29-PRO, 20 Structures===	+	<StructureSection load='2l1z' size='340' side='right' caption='[[2l1z]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>
-		+	== Structural highlights ==
-	==Disease==	+	<table><tr><td colspan='2'>[[2l1z]] 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=2L1Z OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2L1Z FirstGlance]. <br>
-	[[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>	+	</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3oal\|3oal]], [[3ob3\|3ob3]], [[3ob5\|3ob5]], [[2l1y\|2l1y]]</td></tr>
-		+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">INS ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>
-	==Function==	+	<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=2l1z FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2l1z OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2l1z RCSB], [http://www.ebi.ac.uk/pdbsum/2l1z 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.		[[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==
-	[[2l1z]] 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=2L1Z OCA].

	==See Also==		==See Also==
	*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]		*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Hu, S Q.]]	+	[[Category: Hu, S Q]]
-	[[Category: Hua, Q X.]]	+	[[Category: Hua, Q X]]
-	[[Category: Huang, K.]]	+	[[Category: Huang, K]]
-	[[Category: Katsoyannis, J W.]]	+	[[Category: Katsoyannis, J W]]
-	[[Category: Philips, N B.]]	+	[[Category: Philips, N B]]
-	[[Category: Wan, Z L.]]	+	[[Category: Wan, Z L]]
-	[[Category: Weiss, M A.]]	+	[[Category: Weiss, M A]]
	[[Category: Hormone]]		[[Category: Hormone]]
	[[Category: Human insulin]]		[[Category: Human insulin]]
	[[Category: Mutant]]		[[Category: Mutant]]

OCA at 22:04, 24 March 2013

OCA — Sun, 24 Mar 2013 22:04:57 GMT

←Older revision		Revision as of 22:04, 24 March 2013
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-	[[Image:2l1z.png\|left\|200px]]
-
	{{STRUCTURE_2l1z\| PDB=2l1z \| SCENE= }}		{{STRUCTURE_2l1z\| PDB=2l1z \| SCENE= }}
-
	===NMR Structure of human insulin mutant GLY-B20-D-ALA, GLY-B23-D-ALA PRO-B28-LYS, LYS-B29-PRO, 20 Structures===		===NMR Structure of human insulin mutant GLY-B20-D-ALA, GLY-B23-D-ALA PRO-B28-LYS, LYS-B29-PRO, 20 Structures===

		+	==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==		==About this Structure==
Line 11:		Line 13:
	==See Also==		==See Also==
	*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]		*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]
		+
		+	==Reference==
		+	<references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Hu, S Q.]]		[[Category: Hu, S Q.]]

OCA at 15:51, 20 October 2012

OCA — Sat, 20 Oct 2012 15:51:16 GMT

←Older revision		Revision as of 15:51, 20 October 2012
Line 7:		Line 7:

	==About this Structure==		==About this Structure==
-	[[2l1z]] is a 2 chain structure ~~of [[Molecular Playground/Insulin]]~~ 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=2L1Z OCA].	+	[[2l1z]] 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=2L1Z OCA].

	==See Also==		==See Also==

OCA at 19:42, 26 July 2012

OCA — Thu, 26 Jul 2012 19:42:22 GMT

←Older revision		Revision as of 19:42, 26 July 2012
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-	[[Image:2l1z.~~jpg~~\|left\|200px]]	+	[[Image:2l1z.png\|left\|200px]]

-	<!--
-	The line below this paragraph, containing "STRUCTURE_2l1z", creates the "Structure Box" on the page.
-	You may change the PDB parameter (which sets the PDB file loaded into the applet)
-	or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
-	or leave the SCENE parameter empty for the default display.
-	-->
	{{STRUCTURE_2l1z\| PDB=2l1z \| SCENE= }}		{{STRUCTURE_2l1z\| PDB=2l1z \| SCENE= }}

Line 13:		Line 7:

	==About this Structure==		==About this Structure==
-	[[2l1z]] 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=2L1Z OCA].	+	[[2l1z]] is a 2 chain structure of [[Molecular Playground/Insulin]] 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=2L1Z OCA].
		+
		+	==See Also==
		+	*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Hu, S Q.]]		[[Category: Hu, S Q.]]

OCA at 06:51, 31 August 2011

OCA — Wed, 31 Aug 2011 06:51:33 GMT

←Older revision		Revision as of 06:51, 31 August 2011
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-	~~'''Unreleased structure'''~~	+	[[Image:2l1z.jpg\|left\|200px]]

-	The ~~entry 2l1z~~ is ~~ON HOLD~~ ~~until Paper Publication~~	+	<!--
		+	The line below this paragraph, containing "STRUCTURE_2l1z", creates the "Structure Box" on the page.
		+	You may change the PDB parameter (which sets the PDB file loaded into the applet)
		+	or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
		+	or leave the SCENE parameter empty for the default display.
		+	-->
		+	{{STRUCTURE_2l1z\| PDB=2l1z \| SCENE= }}

-	~~Authors: Wan~~, ~~Z.L.~~, ~~Hua~~, ~~Q.X., Huang, K., Hu, S.Q., Philips, N.B., Katsoyannis, J.W., Weiss, M.A.~~	+	===NMR Structure of human insulin mutant GLY-B20-D-ALA, GLY-B23-D-ALA PRO-B28-LYS, LYS-B29-PRO, 20 Structures===

-	~~Description: NMR~~ Structure ~~of human insulin mutant GLY~~-~~B20-D-ALA~~, ~~GLY-B23-D-ALA PRO-B28-LYS~~, ~~LYS-B29-PRO~~, ~~20 Structures~~	+
		+	==About this Structure==
		+	[[2l1z]] 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=2L1Z OCA].
		+	[[Category: Homo sapiens]]
		+	[[Category: Hu, S Q.]]
		+	[[Category: Hua, Q X.]]
		+	[[Category: Huang, K.]]
		+	[[Category: Katsoyannis, J W.]]
		+	[[Category: Philips, N B.]]
		+	[[Category: Wan, Z L.]]
		+	[[Category: Weiss, M A.]]
		+	[[Category: Hormone]]
		+	[[Category: Human insulin]]
		+	[[Category: Mutant]]