2wrx - Revision history

OCA at 10:14, 20 December 2023

OCA — Wed, 20 Dec 2023 10:14:44 GMT

←Older revision		Revision as of 10:14, 20 December 2023
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	<StructureSection load='2wrx' size='340' side='right'caption='[[2wrx]], [[Resolution\|resolution]] 1.50Å' scene=''>		<StructureSection load='2wrx' size='340' side='right'caption='[[2wrx]], [[Resolution\|resolution]] 1.50Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2wrx]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2WRX OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2WRX FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2wrx]] is a 4 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=2WRX OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2WRX FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=NA:SODIUM+ION'>NA</scene>~~</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]] 1.5Å</td></tr>
-	<tr id='~~NonStdRes~~'><td class="sblockLbl"><b>[[~~Non-Standard_Residue~~\|~~NonStd Res~~:]]</b></td><td class="sblockDat"><scene name='pdbligand=MAA:N-METHYL-L-ALANINE'>MAA</scene><~~/td></tr>~~	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=MAA:N-METHYL-L-ALANINE'>MAA</scene>, <scene name='pdbligand=NA:SODIUM+ION'>NA</scene></td></tr>
-	~~<tr id~~='~~related'><td class~~=~~"sblockLbl"><b>[[Related_structure\|Related~~:~~]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;~~'>[[1hit\|1hit]], [[2hho\|2hho]], [[2c8q\|2c8q]], [[1tyl\|1tyl]], [[2c8r\|2c8r]], [[1t1k\|1t1k]], [[1aiy\|1aiy]], [[1xda\|1xda]], [[1htv\|1htv]], [[1mso\|1mso]], [[1uz9\|1uz9]], [[1fub\|1fub]], [[1tym\|1tym]], [[1hui\|1hui]], [[2vk0\|2vk0]], [[1vkt\|1vkt]], [[1hls\|1hls]], [[2ceu\|2ceu]], [[1t1q\|1t1q]], [[1qj0\|1qj0]], [[1mhj\|1mhj]], [[1fu2\|1fu2]], [[1sjt\|1sjt]], [[1qiy\|1qiy]], [[1iog\|1iog]], [[2vjz\|2vjz]], [[1ioh\|1ioh]], [[1trz\|1trz]], [[1evr\|1evr]], [[1ev3\|1ev3]], [[1rwe\|1rwe]], [[1os4\|1os4]], [[1guj\|1guj]], [[1ai0\|1ai0]], [[1sf1\|1sf1]], [[1jco\|1jco]], [[1jca\|1jca]], [[1zeg\|1zeg]], [[1os3\|1os3]], [[1xgl\|1xgl]], [[1t0c\|1t0c]], [[1qiz\|1qiz]], [[1g7b\|1g7b]], [[2wby\|2wby]], [[2aiy\|2aiy]], [[1ev6\|1ev6]], [[1q4v\|1q4v]], [[2hh4\|2hh4]], [[2h67\|2h67]], [[4aiy\|4aiy]], [[1j73\|1j73]], [[1k3m\|1k3m]], [[1mhi\|1mhi]], [[2wc0\|2wc0]], [[2hiu\|2hiu]], [[1kmf\|1kmf]], [[1xw7\|1xw7]], [[5aiy\|5aiy]], [[1g7a\|1g7a]], [[1znj\|1znj]], [[1zeh\|1zeh]], [[1his\|1his]], [[1b9e\|1b9e]], [[3aiy\|3aiy]], [[1w8p\|1w8p]], [[1hiq\|1hiq]], [[1lph\|1lph]], [[1efe\|1efe]], [[1t1p\|1t1p]], [[1a7f\|1a7f]], [[1ben\|1ben]], [[1lkq\|1lkq]], [[2ws7\|2ws7]], [[2ws0\|2ws0]], [[2ws4\|2ws4]], [[2ws1\|2ws1]], [[2ws6\|2ws6]], [[2wrw\|2wrw]], [[2wru\|2wru]], [[2wrv\|2wrv]]</~~div~~></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=2wrx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2wrx OCA], [https://pdbe.org/2wrx PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2wrx RCSB], [https://www.ebi.ac.uk/pdbsum/2wrx PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2wrx 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=2wrx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2wrx OCA], [https://pdbe.org/2wrx PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2wrx RCSB], [https://www.ebi.ac.uk/pdbsum/2wrx PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2wrx 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.
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
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	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Antolikova, E]]	+	[[Category: Antolikova E]]
-	[[Category: Brzozowski~~, A M~~]]	+	[[Category: Brzozowski AM]]
-	[[Category: Dodson~~, G G~~]]	+	[[Category: Dodson GG]]
-	[[Category: Jiracek, J]]	+	[[Category: Jiracek J]]
-	[[Category: Turkenburg~~, J P~~]]	+	[[Category: Turkenburg JP]]
-	[[Category: Watson~~, C J~~]]	+	[[Category: Watson CJ]]
-	[[Category: Zakova, L]]	+	[[Category: Zakova L]]
-	~~[[Category: Analogue]]~~	+
-	~~[[Category: Carbohydrate metabolism]]~~	+
-	~~[[Category: Diabetes mellitus]]~~	+
-	~~[[Category: Glucose metabolism]]~~	+
-	~~[[Category: Hormone~~]]	+

OCA at 11:14, 6 April 2022

OCA — Wed, 06 Apr 2022 11:14:48 GMT

OCA at 09:07, 1 July 2020

OCA — Wed, 01 Jul 2020 09:07:20 GMT

←Older revision		Revision as of 09:07, 1 July 2020
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	==Semi-synthetic analogue of human insulin NMeAlaB26-insulin at pH 3.0==		==Semi-synthetic analogue of human insulin NMeAlaB26-insulin at pH 3.0==
-	<StructureSection load='2wrx' size='340' side='right' caption='[[2wrx]], [[Resolution\|resolution]] 1.50Å' scene=''>	+	<StructureSection load='2wrx' size='340' side='right'caption='[[2wrx]], [[Resolution\|resolution]] 1.50Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2wrx]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2WRX OCA]. For a <b>guided tour on the structure components</b> use [http://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=2WRX FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2wrx]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2WRX OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=2WRX FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=NA:SODIUM+ION'>NA</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=NA:SODIUM+ION'>NA</scene></td></tr>
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MAA:N-METHYL-L-ALANINE'>MAA</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MAA:N-METHYL-L-ALANINE'>MAA</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1hit\|1hit]], [[2hho\|2hho]], [[2c8q\|2c8q]], [[1tyl\|1tyl]], [[2c8r\|2c8r]], [[1t1k\|1t1k]], [[1aiy\|1aiy]], [[1xda\|1xda]], [[1htv\|1htv]], [[1mso\|1mso]], [[1uz9\|1uz9]], [[1fub\|1fub]], [[1tym\|1tym]], [[1hui\|1hui]], [[2vk0\|2vk0]], [[1vkt\|1vkt]], [[1hls\|1hls]], [[2ceu\|2ceu]], [[1t1q\|1t1q]], [[1qj0\|1qj0]], [[1mhj\|1mhj]], [[1fu2\|1fu2]], [[1sjt\|1sjt]], [[1qiy\|1qiy]], [[1iog\|1iog]], [[2vjz\|2vjz]], [[1ioh\|1ioh]], [[1trz\|1trz]], [[1evr\|1evr]], [[1ev3\|1ev3]], [[1rwe\|1rwe]], [[1os4\|1os4]], [[1guj\|1guj]], [[1ai0\|1ai0]], [[1sf1\|1sf1]], [[1jco\|1jco]], [[1jca\|1jca]], [[1zeg\|1zeg]], [[1os3\|1os3]], [[1xgl\|1xgl]], [[1t0c\|1t0c]], [[1qiz\|1qiz]], [[1g7b\|1g7b]], [[2wby\|2wby]], [[2aiy\|2aiy]], [[1ev6\|1ev6]], [[1q4v\|1q4v]], [[2hh4\|2hh4]], [[2h67\|2h67]], [[4aiy\|4aiy]], [[1j73\|1j73]], [[1k3m\|1k3m]], [[1mhi\|1mhi]], [[2wc0\|2wc0]], [[2hiu\|2hiu]], [[1kmf\|1kmf]], [[1xw7\|1xw7]], [[5aiy\|5aiy]], [[1g7a\|1g7a]], [[1znj\|1znj]], [[1zeh\|1zeh]], [[1his\|1his]], [[1b9e\|1b9e]], [[3aiy\|3aiy]], [[1w8p\|1w8p]], [[1hiq\|1hiq]], [[1lph\|1lph]], [[1efe\|1efe]], [[1t1p\|1t1p]], [[1a7f\|1a7f]], [[1ben\|1ben]], [[1lkq\|1lkq]], [[2ws7\|2ws7]], [[2ws0\|2ws0]], [[2ws4\|2ws4]], [[2ws1\|2ws1]], [[2ws6\|2ws6]], [[2wrw\|2wrw]], [[2wru\|2wru]], [[2wrv\|2wrv]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1hit\|1hit]], [[2hho\|2hho]], [[2c8q\|2c8q]], [[1tyl\|1tyl]], [[2c8r\|2c8r]], [[1t1k\|1t1k]], [[1aiy\|1aiy]], [[1xda\|1xda]], [[1htv\|1htv]], [[1mso\|1mso]], [[1uz9\|1uz9]], [[1fub\|1fub]], [[1tym\|1tym]], [[1hui\|1hui]], [[2vk0\|2vk0]], [[1vkt\|1vkt]], [[1hls\|1hls]], [[2ceu\|2ceu]], [[1t1q\|1t1q]], [[1qj0\|1qj0]], [[1mhj\|1mhj]], [[1fu2\|1fu2]], [[1sjt\|1sjt]], [[1qiy\|1qiy]], [[1iog\|1iog]], [[2vjz\|2vjz]], [[1ioh\|1ioh]], [[1trz\|1trz]], [[1evr\|1evr]], [[1ev3\|1ev3]], [[1rwe\|1rwe]], [[1os4\|1os4]], [[1guj\|1guj]], [[1ai0\|1ai0]], [[1sf1\|1sf1]], [[1jco\|1jco]], [[1jca\|1jca]], [[1zeg\|1zeg]], [[1os3\|1os3]], [[1xgl\|1xgl]], [[1t0c\|1t0c]], [[1qiz\|1qiz]], [[1g7b\|1g7b]], [[2wby\|2wby]], [[2aiy\|2aiy]], [[1ev6\|1ev6]], [[1q4v\|1q4v]], [[2hh4\|2hh4]], [[2h67\|2h67]], [[4aiy\|4aiy]], [[1j73\|1j73]], [[1k3m\|1k3m]], [[1mhi\|1mhi]], [[2wc0\|2wc0]], [[2hiu\|2hiu]], [[1kmf\|1kmf]], [[1xw7\|1xw7]], [[5aiy\|5aiy]], [[1g7a\|1g7a]], [[1znj\|1znj]], [[1zeh\|1zeh]], [[1his\|1his]], [[1b9e\|1b9e]], [[3aiy\|3aiy]], [[1w8p\|1w8p]], [[1hiq\|1hiq]], [[1lph\|1lph]], [[1efe\|1efe]], [[1t1p\|1t1p]], [[1a7f\|1a7f]], [[1ben\|1ben]], [[1lkq\|1lkq]], [[2ws7\|2ws7]], [[2ws0\|2ws0]], [[2ws4\|2ws4]], [[2ws1\|2ws1]], [[2ws6\|2ws6]], [[2wrw\|2wrw]], [[2wru\|2wru]], [[2wrv\|2wrv]]</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=2wrx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2wrx OCA], [http://pdbe.org/2wrx PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2wrx RCSB], [http://www.ebi.ac.uk/pdbsum/2wrx PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2wrx 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=2wrx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2wrx OCA], [http://pdbe.org/2wrx PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2wrx RCSB], [http://www.ebi.ac.uk/pdbsum/2wrx PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2wrx ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 34:		Line 34:

	==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: Antolikova, E]]		[[Category: Antolikova, E]]
	[[Category: Brzozowski, A M]]		[[Category: Brzozowski, A M]]

OCA at 08:51, 26 September 2018

OCA — Wed, 26 Sep 2018 08:51:40 GMT

←Older revision		Revision as of 08:51, 26 September 2018
Line 1:		Line 1:
		+
	==Semi-synthetic analogue of human insulin NMeAlaB26-insulin at pH 3.0==		==Semi-synthetic analogue of human insulin NMeAlaB26-insulin at pH 3.0==
	<StructureSection load='2wrx' size='340' side='right' caption='[[2wrx]], [[Resolution\|resolution]] 1.50Å' scene=''>		<StructureSection load='2wrx' size='340' side='right' caption='[[2wrx]], [[Resolution\|resolution]] 1.50Å' scene=''>
Line 6:		Line 7:
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MAA:N-METHYL-L-ALANINE'>MAA</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MAA:N-METHYL-L-ALANINE'>MAA</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1hit\|1hit]], [[2hho\|2hho]], [[2c8q\|2c8q]], [[1tyl\|1tyl]], [[2c8r\|2c8r]], [[1t1k\|1t1k]], [[1aiy\|1aiy]], [[1xda\|1xda]], [[1htv\|1htv]], [[1mso\|1mso]], [[1uz9\|1uz9]], [[1fub\|1fub]], [[1tym\|1tym]], [[1hui\|1hui]], [[2vk0\|2vk0]], [[1vkt\|1vkt]], [[1hls\|1hls]], [[2ceu\|2ceu]], [[1t1q\|1t1q]], [[1qj0\|1qj0]], [[1mhj\|1mhj]], [[1fu2\|1fu2]], [[1sjt\|1sjt]], [[1qiy\|1qiy]], [[1iog\|1iog]], [[2vjz\|2vjz]], [[1ioh\|1ioh]], [[1trz\|1trz]], [[1evr\|1evr]], [[1ev3\|1ev3]], [[1rwe\|1rwe]], [[1os4\|1os4]], [[1guj\|1guj]], [[1ai0\|1ai0]], [[1sf1\|1sf1]], [[1jco\|1jco]], [[1jca\|1jca]], [[1zeg\|1zeg]], [[1os3\|1os3]], [[1xgl\|1xgl]], [[1t0c\|1t0c]], [[1qiz\|1qiz]], [[1g7b\|1g7b]], [[2wby\|2wby]], [[2aiy\|2aiy]], [[1ev6\|1ev6]], [[1q4v\|1q4v]], [[2hh4\|2hh4]], [[2h67\|2h67]], [[4aiy\|4aiy]], [[1j73\|1j73]], [[1k3m\|1k3m]], [[1mhi\|1mhi]], [[2wc0\|2wc0]], [[2hiu\|2hiu]], [[1kmf\|1kmf]], [[1xw7\|1xw7]], [[5aiy\|5aiy]], [[1g7a\|1g7a]], [[1znj\|1znj]], [[1zeh\|1zeh]], [[1his\|1his]], [[1b9e\|1b9e]], [[3aiy\|3aiy]], [[1w8p\|1w8p]], [[1hiq\|1hiq]], [[1lph\|1lph]], [[1efe\|1efe]], [[1t1p\|1t1p]], [[1a7f\|1a7f]], [[1ben\|1ben]], [[1lkq\|1lkq]], [[2ws7\|2ws7]], [[2ws0\|2ws0]], [[2ws4\|2ws4]], [[2ws1\|2ws1]], [[2ws6\|2ws6]], [[2wrw\|2wrw]], [[2wru\|2wru]], [[2wrv\|2wrv]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1hit\|1hit]], [[2hho\|2hho]], [[2c8q\|2c8q]], [[1tyl\|1tyl]], [[2c8r\|2c8r]], [[1t1k\|1t1k]], [[1aiy\|1aiy]], [[1xda\|1xda]], [[1htv\|1htv]], [[1mso\|1mso]], [[1uz9\|1uz9]], [[1fub\|1fub]], [[1tym\|1tym]], [[1hui\|1hui]], [[2vk0\|2vk0]], [[1vkt\|1vkt]], [[1hls\|1hls]], [[2ceu\|2ceu]], [[1t1q\|1t1q]], [[1qj0\|1qj0]], [[1mhj\|1mhj]], [[1fu2\|1fu2]], [[1sjt\|1sjt]], [[1qiy\|1qiy]], [[1iog\|1iog]], [[2vjz\|2vjz]], [[1ioh\|1ioh]], [[1trz\|1trz]], [[1evr\|1evr]], [[1ev3\|1ev3]], [[1rwe\|1rwe]], [[1os4\|1os4]], [[1guj\|1guj]], [[1ai0\|1ai0]], [[1sf1\|1sf1]], [[1jco\|1jco]], [[1jca\|1jca]], [[1zeg\|1zeg]], [[1os3\|1os3]], [[1xgl\|1xgl]], [[1t0c\|1t0c]], [[1qiz\|1qiz]], [[1g7b\|1g7b]], [[2wby\|2wby]], [[2aiy\|2aiy]], [[1ev6\|1ev6]], [[1q4v\|1q4v]], [[2hh4\|2hh4]], [[2h67\|2h67]], [[4aiy\|4aiy]], [[1j73\|1j73]], [[1k3m\|1k3m]], [[1mhi\|1mhi]], [[2wc0\|2wc0]], [[2hiu\|2hiu]], [[1kmf\|1kmf]], [[1xw7\|1xw7]], [[5aiy\|5aiy]], [[1g7a\|1g7a]], [[1znj\|1znj]], [[1zeh\|1zeh]], [[1his\|1his]], [[1b9e\|1b9e]], [[3aiy\|3aiy]], [[1w8p\|1w8p]], [[1hiq\|1hiq]], [[1lph\|1lph]], [[1efe\|1efe]], [[1t1p\|1t1p]], [[1a7f\|1a7f]], [[1ben\|1ben]], [[1lkq\|1lkq]], [[2ws7\|2ws7]], [[2ws0\|2ws0]], [[2ws4\|2ws4]], [[2ws1\|2ws1]], [[2ws6\|2ws6]], [[2wrw\|2wrw]], [[2wru\|2wru]], [[2wrv\|2wrv]]</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=2wrx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2wrx OCA], [http://pdbe.org/2wrx PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2wrx RCSB], [http://www.ebi.ac.uk/pdbsum/2wrx 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=2wrx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2wrx OCA], [http://pdbe.org/2wrx PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2wrx RCSB], [http://www.ebi.ac.uk/pdbsum/2wrx PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2wrx ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 16:		Line 17:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/wr/2wrx_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/wr/2wrx_consurf.spt"</scriptWhenChecked>
	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>		<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>

OCA at 10:04, 7 February 2016

OCA — Sun, 07 Feb 2016 10:04:36 GMT

←Older revision		Revision as of 10:04, 7 February 2016
Line 6:		Line 6:
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MAA:N-METHYL-L-ALANINE'>MAA</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MAA:N-METHYL-L-ALANINE'>MAA</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1hit\|1hit]], [[2hho\|2hho]], [[2c8q\|2c8q]], [[1tyl\|1tyl]], [[2c8r\|2c8r]], [[1t1k\|1t1k]], [[1aiy\|1aiy]], [[1xda\|1xda]], [[1htv\|1htv]], [[1mso\|1mso]], [[1uz9\|1uz9]], [[1fub\|1fub]], [[1tym\|1tym]], [[1hui\|1hui]], [[2vk0\|2vk0]], [[1vkt\|1vkt]], [[1hls\|1hls]], [[2ceu\|2ceu]], [[1t1q\|1t1q]], [[1qj0\|1qj0]], [[1mhj\|1mhj]], [[1fu2\|1fu2]], [[1sjt\|1sjt]], [[1qiy\|1qiy]], [[1iog\|1iog]], [[2vjz\|2vjz]], [[1ioh\|1ioh]], [[1trz\|1trz]], [[1evr\|1evr]], [[1ev3\|1ev3]], [[1rwe\|1rwe]], [[1os4\|1os4]], [[1guj\|1guj]], [[1ai0\|1ai0]], [[1sf1\|1sf1]], [[1jco\|1jco]], [[1jca\|1jca]], [[1zeg\|1zeg]], [[1os3\|1os3]], [[1xgl\|1xgl]], [[1t0c\|1t0c]], [[1qiz\|1qiz]], [[1g7b\|1g7b]], [[2wby\|2wby]], [[2aiy\|2aiy]], [[1ev6\|1ev6]], [[1q4v\|1q4v]], [[2hh4\|2hh4]], [[2h67\|2h67]], [[4aiy\|4aiy]], [[1j73\|1j73]], [[1k3m\|1k3m]], [[1mhi\|1mhi]], [[2wc0\|2wc0]], [[2hiu\|2hiu]], [[1kmf\|1kmf]], [[1xw7\|1xw7]], [[5aiy\|5aiy]], [[1g7a\|1g7a]], [[1znj\|1znj]], [[1zeh\|1zeh]], [[1his\|1his]], [[1b9e\|1b9e]], [[3aiy\|3aiy]], [[1w8p\|1w8p]], [[1hiq\|1hiq]], [[1lph\|1lph]], [[1efe\|1efe]], [[1t1p\|1t1p]], [[1a7f\|1a7f]], [[1ben\|1ben]], [[1lkq\|1lkq]], [[2ws7\|2ws7]], [[2ws0\|2ws0]], [[2ws4\|2ws4]], [[2ws1\|2ws1]], [[2ws6\|2ws6]], [[2wrw\|2wrw]], [[2wru\|2wru]], [[2wrv\|2wrv]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1hit\|1hit]], [[2hho\|2hho]], [[2c8q\|2c8q]], [[1tyl\|1tyl]], [[2c8r\|2c8r]], [[1t1k\|1t1k]], [[1aiy\|1aiy]], [[1xda\|1xda]], [[1htv\|1htv]], [[1mso\|1mso]], [[1uz9\|1uz9]], [[1fub\|1fub]], [[1tym\|1tym]], [[1hui\|1hui]], [[2vk0\|2vk0]], [[1vkt\|1vkt]], [[1hls\|1hls]], [[2ceu\|2ceu]], [[1t1q\|1t1q]], [[1qj0\|1qj0]], [[1mhj\|1mhj]], [[1fu2\|1fu2]], [[1sjt\|1sjt]], [[1qiy\|1qiy]], [[1iog\|1iog]], [[2vjz\|2vjz]], [[1ioh\|1ioh]], [[1trz\|1trz]], [[1evr\|1evr]], [[1ev3\|1ev3]], [[1rwe\|1rwe]], [[1os4\|1os4]], [[1guj\|1guj]], [[1ai0\|1ai0]], [[1sf1\|1sf1]], [[1jco\|1jco]], [[1jca\|1jca]], [[1zeg\|1zeg]], [[1os3\|1os3]], [[1xgl\|1xgl]], [[1t0c\|1t0c]], [[1qiz\|1qiz]], [[1g7b\|1g7b]], [[2wby\|2wby]], [[2aiy\|2aiy]], [[1ev6\|1ev6]], [[1q4v\|1q4v]], [[2hh4\|2hh4]], [[2h67\|2h67]], [[4aiy\|4aiy]], [[1j73\|1j73]], [[1k3m\|1k3m]], [[1mhi\|1mhi]], [[2wc0\|2wc0]], [[2hiu\|2hiu]], [[1kmf\|1kmf]], [[1xw7\|1xw7]], [[5aiy\|5aiy]], [[1g7a\|1g7a]], [[1znj\|1znj]], [[1zeh\|1zeh]], [[1his\|1his]], [[1b9e\|1b9e]], [[3aiy\|3aiy]], [[1w8p\|1w8p]], [[1hiq\|1hiq]], [[1lph\|1lph]], [[1efe\|1efe]], [[1t1p\|1t1p]], [[1a7f\|1a7f]], [[1ben\|1ben]], [[1lkq\|1lkq]], [[2ws7\|2ws7]], [[2ws0\|2ws0]], [[2ws4\|2ws4]], [[2ws1\|2ws1]], [[2ws6\|2ws6]], [[2wrw\|2wrw]], [[2wru\|2wru]], [[2wrv\|2wrv]]</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=2wrx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2wrx OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2wrx RCSB], [http://www.ebi.ac.uk/pdbsum/2wrx 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=2wrx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2wrx OCA], [http://pdbe.org/2wrx PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2wrx RCSB], [http://www.ebi.ac.uk/pdbsum/2wrx PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 20:		Line 20:
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>
	</jmolCheckbox>		</jmolCheckbox>
-	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/~~chain_selection~~.php?pdb_ID=~~2ata~~ ConSurf].	+	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=2wrx ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
Line 30:		Line 30:
	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 2wrx" style="background-color:#fffaf0;"></div>

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

OCA at 07:39, 20 January 2015

OCA — Tue, 20 Jan 2015 07:39:08 GMT

←Older revision		Revision as of 07:39, 20 January 2015
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2wrx]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2WRX OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2WRX FirstGlance]. <br>		<table><tr><td colspan='2'>[[2wrx]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2WRX OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2WRX FirstGlance]. <br>
-	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=NA:SODIUM+ION'>NA</scene><br>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=NA:SODIUM+ION'>NA</scene></td></tr>
-	<tr><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MAA:N-METHYL-L-ALANINE'>MAA</scene></td></tr>	+	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MAA:N-METHYL-L-ALANINE'>MAA</scene></td></tr>
-	<tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1hit\|1hit]], [[2hho\|2hho]], [[2c8q\|2c8q]], [[1tyl\|1tyl]], [[2c8r\|2c8r]], [[1t1k\|1t1k]], [[1aiy\|1aiy]], [[1xda\|1xda]], [[1htv\|1htv]], [[1mso\|1mso]], [[1uz9\|1uz9]], [[1fub\|1fub]], [[1tym\|1tym]], [[1hui\|1hui]], [[2vk0\|2vk0]], [[1vkt\|1vkt]], [[1hls\|1hls]], [[2ceu\|2ceu]], [[1t1q\|1t1q]], [[1qj0\|1qj0]], [[1mhj\|1mhj]], [[1fu2\|1fu2]], [[1sjt\|1sjt]], [[1qiy\|1qiy]], [[1iog\|1iog]], [[2vjz\|2vjz]], [[1ioh\|1ioh]], [[1trz\|1trz]], [[1evr\|1evr]], [[1ev3\|1ev3]], [[1rwe\|1rwe]], [[1os4\|1os4]], [[1guj\|1guj]], [[1ai0\|1ai0]], [[1sf1\|1sf1]], [[1jco\|1jco]], [[1jca\|1jca]], [[1zeg\|1zeg]], [[1os3\|1os3]], [[1xgl\|1xgl]], [[1t0c\|1t0c]], [[1qiz\|1qiz]], [[1g7b\|1g7b]], [[2wby\|2wby]], [[2aiy\|2aiy]], [[1ev6\|1ev6]], [[1q4v\|1q4v]], [[2hh4\|2hh4]], [[2h67\|2h67]], [[4aiy\|4aiy]], [[1j73\|1j73]], [[1k3m\|1k3m]], [[1mhi\|1mhi]], [[2wc0\|2wc0]], [[2hiu\|2hiu]], [[1kmf\|1kmf]], [[1xw7\|1xw7]], [[5aiy\|5aiy]], [[1g7a\|1g7a]], [[1znj\|1znj]], [[1zeh\|1zeh]], [[1his\|1his]], [[1b9e\|1b9e]], [[3aiy\|3aiy]], [[1w8p\|1w8p]], [[1hiq\|1hiq]], [[1lph\|1lph]], [[1efe\|1efe]], [[1t1p\|1t1p]], [[1a7f\|1a7f]], [[1ben\|1ben]], [[1lkq\|1lkq]], [[2ws7\|2ws7]], [[2ws0\|2ws0]], [[2ws4\|2ws4]], [[2ws1\|2ws1]], [[2ws6\|2ws6]], [[2wrw\|2wrw]], [[2wru\|2wru]], [[2wrv\|2wrv]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1hit\|1hit]], [[2hho\|2hho]], [[2c8q\|2c8q]], [[1tyl\|1tyl]], [[2c8r\|2c8r]], [[1t1k\|1t1k]], [[1aiy\|1aiy]], [[1xda\|1xda]], [[1htv\|1htv]], [[1mso\|1mso]], [[1uz9\|1uz9]], [[1fub\|1fub]], [[1tym\|1tym]], [[1hui\|1hui]], [[2vk0\|2vk0]], [[1vkt\|1vkt]], [[1hls\|1hls]], [[2ceu\|2ceu]], [[1t1q\|1t1q]], [[1qj0\|1qj0]], [[1mhj\|1mhj]], [[1fu2\|1fu2]], [[1sjt\|1sjt]], [[1qiy\|1qiy]], [[1iog\|1iog]], [[2vjz\|2vjz]], [[1ioh\|1ioh]], [[1trz\|1trz]], [[1evr\|1evr]], [[1ev3\|1ev3]], [[1rwe\|1rwe]], [[1os4\|1os4]], [[1guj\|1guj]], [[1ai0\|1ai0]], [[1sf1\|1sf1]], [[1jco\|1jco]], [[1jca\|1jca]], [[1zeg\|1zeg]], [[1os3\|1os3]], [[1xgl\|1xgl]], [[1t0c\|1t0c]], [[1qiz\|1qiz]], [[1g7b\|1g7b]], [[2wby\|2wby]], [[2aiy\|2aiy]], [[1ev6\|1ev6]], [[1q4v\|1q4v]], [[2hh4\|2hh4]], [[2h67\|2h67]], [[4aiy\|4aiy]], [[1j73\|1j73]], [[1k3m\|1k3m]], [[1mhi\|1mhi]], [[2wc0\|2wc0]], [[2hiu\|2hiu]], [[1kmf\|1kmf]], [[1xw7\|1xw7]], [[5aiy\|5aiy]], [[1g7a\|1g7a]], [[1znj\|1znj]], [[1zeh\|1zeh]], [[1his\|1his]], [[1b9e\|1b9e]], [[3aiy\|3aiy]], [[1w8p\|1w8p]], [[1hiq\|1hiq]], [[1lph\|1lph]], [[1efe\|1efe]], [[1t1p\|1t1p]], [[1a7f\|1a7f]], [[1ben\|1ben]], [[1lkq\|1lkq]], [[2ws7\|2ws7]], [[2ws0\|2ws0]], [[2ws4\|2ws4]], [[2ws1\|2ws1]], [[2ws6\|2ws6]], [[2wrw\|2wrw]], [[2wru\|2wru]], [[2wrv\|2wrv]]</td></tr>
-	<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2wrx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2wrx OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2wrx RCSB], [http://www.ebi.ac.uk/pdbsum/2wrx 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=2wrx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2wrx OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2wrx RCSB], [http://www.ebi.ac.uk/pdbsum/2wrx PDBsum]</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>		[[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>
Line 37:		Line 37:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: Antolikova, E.]]	+	[[Category: Antolikova, E]]
-	[[Category: Brzozowski, A M.]]	+	[[Category: Brzozowski, A M]]
-	[[Category: Dodson, G G.]]	+	[[Category: Dodson, G G]]
-	[[Category: Jiracek, J.]]	+	[[Category: Jiracek, J]]
-	[[Category: Turkenburg, J P.]]	+	[[Category: Turkenburg, J P]]
-	[[Category: Watson, C J.]]	+	[[Category: Watson, C J]]
-	[[Category: Zakova, L.]]	+	[[Category: Zakova, L]]
	[[Category: Analogue]]		[[Category: Analogue]]
	[[Category: Carbohydrate metabolism]]		[[Category: Carbohydrate metabolism]]

OCA at 01:11, 1 October 2014

OCA — Wed, 01 Oct 2014 01:11:23 GMT

←Older revision		Revision as of 01:11, 1 October 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_2wrx\| PDB=2wrx \| SCENE= }}~~	+	==Semi-synthetic analogue of human insulin NMeAlaB26-insulin at pH 3.0==
-	===Semi-synthetic analogue of human insulin NMeAlaB26-insulin at pH 3.0===	+	<StructureSection load='2wrx' size='340' side='right' caption='[[2wrx]], [[Resolution\|resolution]] 1.50Å' scene=''>
-	~~{{ABSTRACT_PUBMED_20133841}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[2wrx]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2WRX OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2WRX FirstGlance]. <br>
		+	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=NA:SODIUM+ION'>NA</scene><br>
		+	<tr><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MAA:N-METHYL-L-ALANINE'>MAA</scene></td></tr>
		+	<tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1hit\|1hit]], [[2hho\|2hho]], [[2c8q\|2c8q]], [[1tyl\|1tyl]], [[2c8r\|2c8r]], [[1t1k\|1t1k]], [[1aiy\|1aiy]], [[1xda\|1xda]], [[1htv\|1htv]], [[1mso\|1mso]], [[1uz9\|1uz9]], [[1fub\|1fub]], [[1tym\|1tym]], [[1hui\|1hui]], [[2vk0\|2vk0]], [[1vkt\|1vkt]], [[1hls\|1hls]], [[2ceu\|2ceu]], [[1t1q\|1t1q]], [[1qj0\|1qj0]], [[1mhj\|1mhj]], [[1fu2\|1fu2]], [[1sjt\|1sjt]], [[1qiy\|1qiy]], [[1iog\|1iog]], [[2vjz\|2vjz]], [[1ioh\|1ioh]], [[1trz\|1trz]], [[1evr\|1evr]], [[1ev3\|1ev3]], [[1rwe\|1rwe]], [[1os4\|1os4]], [[1guj\|1guj]], [[1ai0\|1ai0]], [[1sf1\|1sf1]], [[1jco\|1jco]], [[1jca\|1jca]], [[1zeg\|1zeg]], [[1os3\|1os3]], [[1xgl\|1xgl]], [[1t0c\|1t0c]], [[1qiz\|1qiz]], [[1g7b\|1g7b]], [[2wby\|2wby]], [[2aiy\|2aiy]], [[1ev6\|1ev6]], [[1q4v\|1q4v]], [[2hh4\|2hh4]], [[2h67\|2h67]], [[4aiy\|4aiy]], [[1j73\|1j73]], [[1k3m\|1k3m]], [[1mhi\|1mhi]], [[2wc0\|2wc0]], [[2hiu\|2hiu]], [[1kmf\|1kmf]], [[1xw7\|1xw7]], [[5aiy\|5aiy]], [[1g7a\|1g7a]], [[1znj\|1znj]], [[1zeh\|1zeh]], [[1his\|1his]], [[1b9e\|1b9e]], [[3aiy\|3aiy]], [[1w8p\|1w8p]], [[1hiq\|1hiq]], [[1lph\|1lph]], [[1efe\|1efe]], [[1t1p\|1t1p]], [[1a7f\|1a7f]], [[1ben\|1ben]], [[1lkq\|1lkq]], [[2ws7\|2ws7]], [[2ws0\|2ws0]], [[2ws4\|2ws4]], [[2ws1\|2ws1]], [[2ws6\|2ws6]], [[2wrw\|2wrw]], [[2wru\|2wru]], [[2wrv\|2wrv]]</td></tr>
		+	<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2wrx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2wrx OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2wrx RCSB], [http://www.ebi.ac.uk/pdbsum/2wrx 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.
		+	== Evolutionary Conservation ==
		+	[[Image:Consurf_key_small.gif\|200px\|right]]
		+	Check<jmol>
		+	<jmolCheckbox>
		+	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/wr/2wrx_consurf.spt"</scriptWhenChecked>
		+	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
		+	<text>to colour the structure by Evolutionary Conservation</text>
		+	</jmolCheckbox>
		+	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/chain_selection.php?pdb_ID=2ata ConSurf].
		+	<div style="clear:both"></div>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Insulin is a key protein hormone that regulates blood glucose levels and, thus, has widespread impact on lipid and protein metabolism. Insulin action is manifested through binding of its monomeric form to the Insulin Receptor (IR). At present, however, our knowledge about the structural behavior of insulin is based upon inactive, multimeric, and storage-like states. The active monomeric structure, when in complex with the receptor, must be different as the residues crucial for the interactions are buried within the multimeric forms. Although the exact nature of the insulin's induced-fit is unknown, there is strong evidence that the C-terminal part of the B-chain is a dynamic element in insulin activation and receptor binding. Here, we present the design and analysis of highly active (200-500%) insulin analogues that are truncated at residue 26 of the B-chain (B(26)). They show a structural convergence in the form of a new beta-turn at B(24)-B(26). We propose that the key element in insulin's transition, from an inactive to an active state, may be the formation of the beta-turn at B(24)-B(26) associated with a trans to cis isomerisation at the B(25)-B(26) peptide bond. Here, this turn is achieved with N-methylated L-amino acids adjacent to the trans to cis switch at the B(25)-B(26) peptide bond or by the insertion of certain D-amino acids at B(26). The resultant conformational changes unmask previously buried amino acids that are implicated in IR binding and provide structural details for new approaches in rational design of ligands effective in combating diabetes.

-	~~==Disease==~~	+	Implications for the active form of human insulin based on the structural convergence of highly active hormone analogues.,Jiracek J, Zakova L, Antolikova E, Watson CJ, Turkenburg JP, Dodson GG, Brzozowski AM Proc Natl Acad Sci U S A. 2010 Feb 2;107(5):1966-70. Epub 2010 Jan 25. PMID:20133841<ref>PMID:20133841</ref>
-	~~[[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==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[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>
-		+
-	~~==About this Structure==~~	+
-	~~[[2wrx]] is a 4 chain structure~~. ~~Full crystallographic information is available from [http://oca~~.~~weizmann.ac.il~~/~~oca-bin/ocashort?id=2WRX OCA].~~	+

	==See Also==		==See Also==
	*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]		*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:020133841</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Antolikova, E.]]		[[Category: Antolikova, E.]]
	[[Category: Brzozowski, A M.]]		[[Category: Brzozowski, A M.]]

OCA at 18:07, 24 March 2013

OCA — Sun, 24 Mar 2013 18:07:47 GMT

←Older revision		Revision as of 18:07, 24 March 2013
Line 1:		Line 1:
-	[[Image:2wrx.png\|left\|200px]]
-
	{{STRUCTURE_2wrx\| PDB=2wrx \| SCENE= }}		{{STRUCTURE_2wrx\| PDB=2wrx \| SCENE= }}
-
	===Semi-synthetic analogue of human insulin NMeAlaB26-insulin at pH 3.0===		===Semi-synthetic analogue of human insulin NMeAlaB26-insulin at pH 3.0===
		+	{{ABSTRACT_PUBMED_20133841}}

-	~~{{ABSTRACT_PUBMED_20133841}}~~	+	==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 14:		Line 16:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:020133841</ref><references group="xtra"/>	+	<ref group="xtra">PMID:020133841</ref><references group="xtra"/><references/>
	[[Category: Antolikova, E.]]		[[Category: Antolikova, E.]]
	[[Category: Brzozowski, A M.]]		[[Category: Brzozowski, A M.]]

OCA at 06:19, 20 October 2012

OCA — Sat, 20 Oct 2012 06:19:16 GMT

←Older revision		Revision as of 06:19, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[2wrx]] is a 4 chain structure ~~of [[Molecular Playground/Insulin]]~~. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2WRX OCA].	+	[[2wrx]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2WRX OCA].

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

OCA at 12:48, 25 July 2012

OCA — Wed, 25 Jul 2012 12:48:20 GMT

←Older revision		Revision as of 12:48, 25 July 2012
Line 1:		Line 1:
	[[Image:2wrx.png\|left\|200px]]		[[Image:2wrx.png\|left\|200px]]

-	<!--
-	The line below this paragraph, containing "STRUCTURE_2wrx", 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_2wrx\| PDB=2wrx \| SCENE= }}		{{STRUCTURE_2wrx\| PDB=2wrx \| SCENE= }}

	===Semi-synthetic analogue of human insulin NMeAlaB26-insulin at pH 3.0===		===Semi-synthetic analogue of human insulin NMeAlaB26-insulin at pH 3.0===

-
-	<!--
-	The line below this paragraph, {{ABSTRACT_PUBMED_20133841}}, adds the Publication Abstract to the page
-	(as it appears on PubMed at http://www.pubmed.gov), where 20133841 is the PubMed ID number.
-	-->
	{{ABSTRACT_PUBMED_20133841}}		{{ABSTRACT_PUBMED_20133841}}

←Older revision		Revision as of 11:14, 6 April 2022
Line 3:		Line 3:
	<StructureSection load='2wrx' size='340' side='right'caption='[[2wrx]], [[Resolution\|resolution]] 1.50Å' scene=''>		<StructureSection load='2wrx' size='340' side='right'caption='[[2wrx]], [[Resolution\|resolution]] 1.50Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2wrx]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2WRX OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://proteopedia.org/fgij/fg.htm?mol=2WRX FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2wrx]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2WRX OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2WRX FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=NA:SODIUM+ION'>NA</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=NA:SODIUM+ION'>NA</scene></td></tr>
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MAA:N-METHYL-L-ALANINE'>MAA</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MAA:N-METHYL-L-ALANINE'>MAA</scene></td></tr>
-	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1hit\|1hit]], [[2hho\|2hho]], [[2c8q\|2c8q]], [[1tyl\|1tyl]], [[2c8r\|2c8r]], [[1t1k\|1t1k]], [[1aiy\|1aiy]], [[1xda\|1xda]], [[1htv\|1htv]], [[1mso\|1mso]], [[1uz9\|1uz9]], [[1fub\|1fub]], [[1tym\|1tym]], [[1hui\|1hui]], [[2vk0\|2vk0]], [[1vkt\|1vkt]], [[1hls\|1hls]], [[2ceu\|2ceu]], [[1t1q\|1t1q]], [[1qj0\|1qj0]], [[1mhj\|1mhj]], [[1fu2\|1fu2]], [[1sjt\|1sjt]], [[1qiy\|1qiy]], [[1iog\|1iog]], [[2vjz\|2vjz]], [[1ioh\|1ioh]], [[1trz\|1trz]], [[1evr\|1evr]], [[1ev3\|1ev3]], [[1rwe\|1rwe]], [[1os4\|1os4]], [[1guj\|1guj]], [[1ai0\|1ai0]], [[1sf1\|1sf1]], [[1jco\|1jco]], [[1jca\|1jca]], [[1zeg\|1zeg]], [[1os3\|1os3]], [[1xgl\|1xgl]], [[1t0c\|1t0c]], [[1qiz\|1qiz]], [[1g7b\|1g7b]], [[2wby\|2wby]], [[2aiy\|2aiy]], [[1ev6\|1ev6]], [[1q4v\|1q4v]], [[2hh4\|2hh4]], [[2h67\|2h67]], [[4aiy\|4aiy]], [[1j73\|1j73]], [[1k3m\|1k3m]], [[1mhi\|1mhi]], [[2wc0\|2wc0]], [[2hiu\|2hiu]], [[1kmf\|1kmf]], [[1xw7\|1xw7]], [[5aiy\|5aiy]], [[1g7a\|1g7a]], [[1znj\|1znj]], [[1zeh\|1zeh]], [[1his\|1his]], [[1b9e\|1b9e]], [[3aiy\|3aiy]], [[1w8p\|1w8p]], [[1hiq\|1hiq]], [[1lph\|1lph]], [[1efe\|1efe]], [[1t1p\|1t1p]], [[1a7f\|1a7f]], [[1ben\|1ben]], [[1lkq\|1lkq]], [[2ws7\|2ws7]], [[2ws0\|2ws0]], [[2ws4\|2ws4]], [[2ws1\|2ws1]], [[2ws6\|2ws6]], [[2wrw\|2wrw]], [[2wru\|2wru]], [[2wrv\|2wrv]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[1hit\|1hit]], [[2hho\|2hho]], [[2c8q\|2c8q]], [[1tyl\|1tyl]], [[2c8r\|2c8r]], [[1t1k\|1t1k]], [[1aiy\|1aiy]], [[1xda\|1xda]], [[1htv\|1htv]], [[1mso\|1mso]], [[1uz9\|1uz9]], [[1fub\|1fub]], [[1tym\|1tym]], [[1hui\|1hui]], [[2vk0\|2vk0]], [[1vkt\|1vkt]], [[1hls\|1hls]], [[2ceu\|2ceu]], [[1t1q\|1t1q]], [[1qj0\|1qj0]], [[1mhj\|1mhj]], [[1fu2\|1fu2]], [[1sjt\|1sjt]], [[1qiy\|1qiy]], [[1iog\|1iog]], [[2vjz\|2vjz]], [[1ioh\|1ioh]], [[1trz\|1trz]], [[1evr\|1evr]], [[1ev3\|1ev3]], [[1rwe\|1rwe]], [[1os4\|1os4]], [[1guj\|1guj]], [[1ai0\|1ai0]], [[1sf1\|1sf1]], [[1jco\|1jco]], [[1jca\|1jca]], [[1zeg\|1zeg]], [[1os3\|1os3]], [[1xgl\|1xgl]], [[1t0c\|1t0c]], [[1qiz\|1qiz]], [[1g7b\|1g7b]], [[2wby\|2wby]], [[2aiy\|2aiy]], [[1ev6\|1ev6]], [[1q4v\|1q4v]], [[2hh4\|2hh4]], [[2h67\|2h67]], [[4aiy\|4aiy]], [[1j73\|1j73]], [[1k3m\|1k3m]], [[1mhi\|1mhi]], [[2wc0\|2wc0]], [[2hiu\|2hiu]], [[1kmf\|1kmf]], [[1xw7\|1xw7]], [[5aiy\|5aiy]], [[1g7a\|1g7a]], [[1znj\|1znj]], [[1zeh\|1zeh]], [[1his\|1his]], [[1b9e\|1b9e]], [[3aiy\|3aiy]], [[1w8p\|1w8p]], [[1hiq\|1hiq]], [[1lph\|1lph]], [[1efe\|1efe]], [[1t1p\|1t1p]], [[1a7f\|1a7f]], [[1ben\|1ben]], [[1lkq\|1lkq]], [[2ws7\|2ws7]], [[2ws0\|2ws0]], [[2ws4\|2ws4]], [[2ws1\|2ws1]], [[2ws6\|2ws6]], [[2wrw\|2wrw]], [[2wru\|2wru]], [[2wrv\|2wrv]]</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=2wrx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2wrx OCA], [~~http~~://pdbe.org/2wrx PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=2wrx RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/2wrx PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=2wrx 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=2wrx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2wrx OCA], [https://pdbe.org/2wrx PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2wrx RCSB], [https://www.ebi.ac.uk/pdbsum/2wrx PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2wrx 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.
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]