3zqr - Revision history

OCA at 11:10, 20 December 2023

2023-12-20T11:10:14Z

←Older revision		Revision as of 11:10, 20 December 2023
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	<StructureSection load='3zqr' size='340' side='right'caption='[[3zqr]], [[Resolution\|resolution]] 1.90Å' scene=''>		<StructureSection load='3zqr' size='340' side='right'caption='[[3zqr]], [[Resolution\|resolution]] 1.90Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3zqr]] is a 12 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3ZQR OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3ZQR FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3zqr]] is a 12 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=3ZQR OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3ZQR FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>~~, ~~<scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</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]] 1.9Å</td></tr>
-	<tr id='~~NonStdRes~~'><td class="sblockLbl"><b>[[~~Non-Standard_Residue~~\|~~NonStd Res~~:]]</b></td><td class="sblockDat"><scene name='pdbligand=~~MEA~~:~~N-METHYLPHENYLALANINE~~'>~~MEA~~</scene><~~/td~~></tr>	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=MEA:N-METHYLPHENYLALANINE'>MEA</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</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]], [[2w44\|2w44]], [[1tyl\|1tyl]], [[2c8r\|2c8r]], [[1t1k\|1t1k]], [[2wrv\|2wrv]], [[1aiy\|1aiy]], [[1xda\|1xda]], [[1htv\|1htv]], [[1mso\|1mso]], [[1uz9\|1uz9]], [[2ws6\|2ws6]], [[1fub\|1fub]], [[1tym\|1tym]], [[1hui\|1hui]], [[2vk0\|2vk0]], [[1vkt\|1vkt]], [[1hls\|1hls]], [[2ceu\|2ceu]], [[1t1q\|1t1q]], [[1qj0\|1qj0]], [[2ws0\|2ws0]], [[1mhj\|1mhj]], [[1fu2\|1fu2]], [[1sjt\|1sjt]], [[1qiy\|1qiy]], [[1iog\|1iog]], [[2vjz\|2vjz]], [[1ioh\|1ioh]], [[1trz\|1trz]], [[1evr\|1evr]], [[1sju\|1sju]], [[1ev3\|1ev3]], [[1rwe\|1rwe]], [[1os4\|1os4]], [[1guj\|1guj]], [[1ai0\|1ai0]], [[1sf1\|1sf1]], [[1jco\|1jco]], [[1jca\|1jca]], [[1zeg\|1zeg]], [[1os3\|1os3]], [[1xgl\|1xgl]], [[1qiz\|1qiz]], [[1t0c\|1t0c]], [[1g7b\|1g7b]], [[2wby\|2wby]], [[2aiy\|2aiy]], [[1ev6\|1ev6]], [[1q4v\|1q4v]], [[2ws7\|2ws7]], [[2hh4\|2hh4]], [[2h67\|2h67]], [[4aiy\|4aiy]], [[1j73\|1j73]], [[1k3m\|1k3m]], [[1mhi\|1mhi]], [[2wc0\|2wc0]], [[1kmf\|1kmf]], [[2hiu\|2hiu]], [[1xw7\|1xw7]], [[2wrw\|2wrw]], [[5aiy\|5aiy]], [[1g7a\|1g7a]], [[1znj\|1znj]], [[2ws4\|2ws4]], [[1zeh\|1zeh]], [[1his\|1his]], [[1b9e\|1b9e]], [[3aiy\|3aiy]], [[1w8p\|1w8p]], [[2ws1\|2ws1]], [[2wrx\|2wrx]], [[1hiq\|1hiq]], [[1lph\|1lph]], [[1efe\|1efe]], [[1a7f\|1a7f]], [[1t1p\|1t1p]], [[1ben\|1ben]], [[2wru\|2wru]], [[1lkq\|1lkq]]</~~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=3zqr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3zqr OCA], [https://pdbe.org/3zqr PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3zqr RCSB], [https://www.ebi.ac.uk/pdbsum/3zqr PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3zqr 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=3zqr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3zqr OCA], [https://pdbe.org/3zqr PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3zqr RCSB], [https://www.ebi.ac.uk/pdbsum/3zqr PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3zqr ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Defects in INS are the cause of familial hyperproinsulinemia (FHPRI) [MIM:[https://omim.org/entry/176730 176730]].<ref>PMID:3470784</ref> <ref>PMID:2196279</ref> <ref>PMID:4019786</ref> <ref>PMID:1601997</ref> Defects in INS are a cause of diabetes mellitus insulin-dependent type 2 (IDDM2) [MIM:[https://omim.org/entry/125852 125852]]. IDDM2 is a multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Clinical fetaures are polydipsia, polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.<ref>PMID:18192540</ref> Defects in INS are a cause of diabetes mellitus permanent neonatal (PNDM) [MIM:[https://omim.org/entry/606176 606176]]. PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy.<ref>PMID:17855560</ref> <ref>PMID:18162506</ref> Defects in INS are a cause of maturity-onset diabetes of the young type 10 (MODY10) [MIM:[https://omim.org/entry/613370 613370]]. MODY10 is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.<ref>PMID:18192540</ref> <ref>PMID:18162506</ref> <ref>PMID:20226046</ref>	+	[https://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN] Defects in INS are the cause of familial hyperproinsulinemia (FHPRI) [MIM:[https://omim.org/entry/176730 176730].<ref>PMID:3470784</ref> <ref>PMID:2196279</ref> <ref>PMID:4019786</ref> <ref>PMID:1601997</ref> Defects in INS are a cause of diabetes mellitus insulin-dependent type 2 (IDDM2) [MIM:[https://omim.org/entry/125852 125852]. IDDM2 is a multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Clinical fetaures are polydipsia, polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.<ref>PMID:18192540</ref> Defects in INS are a cause of diabetes mellitus permanent neonatal (PNDM) [MIM:[https://omim.org/entry/606176 606176]. PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy.<ref>PMID:17855560</ref> <ref>PMID:18162506</ref> Defects in INS are a cause of maturity-onset diabetes of the young type 10 (MODY10) [MIM:[https://omim.org/entry/613370 613370]. MODY10 is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.<ref>PMID:18192540</ref> <ref>PMID:18162506</ref> <ref>PMID:20226046</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver.	+	[https://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN] Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver.
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
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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: Cooper, A]]	+	[[Category: Cooper A]]
-	[[Category: Hanclova, I]]	+	[[Category: Hanclova I]]
-	[[Category: Jiracek~~, J A~~]]	+	[[Category: Jiracek JA]]
-	[[Category: Kraus, T]]	+	[[Category: Kraus T]]
-	[[Category: Sanda, M]]	+	[[Category: Sanda M]]
-	[[Category: Turkenburg~~, J P~~]]	+	[[Category: Turkenburg JP]]
-	[[Category: Watson~~, C J~~]]	+	[[Category: Watson CJ]]
-	[[Category: Zakova, L]]	+	[[Category: Zakova L]]
-	~~[[Category: Carbohydrate metabolism]]~~	+
-	~~[[Category: Diabetes mellitus]]~~	+
-	~~[[Category: Glucose metabolism]]~~	+
-	~~[[Category: Hormone~~]]	+

OCA at 07:10, 18 August 2022

2022-08-18T07:10:44Z

OCA at 07:16, 7 August 2019

2019-08-07T07:16:37Z

←Older revision		Revision as of 07:16, 7 August 2019
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	==NMePheB25 insulin analogue crystal structure==		==NMePheB25 insulin analogue crystal structure==
-	<StructureSection load='3zqr' size='340' side='right' caption='[[3zqr]], [[Resolution\|resolution]] 1.90Å' scene=''>	+	<StructureSection load='3zqr' size='340' side='right'caption='[[3zqr]], [[Resolution\|resolution]] 1.90Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[3zqr]] is a 12 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3ZQR OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3ZQR FirstGlance]. <br>		<table><tr><td colspan='2'>[[3zqr]] is a 12 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3ZQR OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3ZQR FirstGlance]. <br>
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	</div>		</div>
	<div class="pdbe-citations 3zqr" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 3zqr" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[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 12:24, 6 November 2017

2017-11-06T12:24:26Z

←Older revision		Revision as of 12:24, 6 November 2017
Line 22:		Line 22:
	</div>		</div>
	<div class="pdbe-citations 3zqr" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 3zqr" style="background-color:#fffaf0;"></div>
-
-	==See Also==
-	*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 11:46, 3 August 2017

2017-08-03T11:46:04Z

←Older revision		Revision as of 11:46, 3 August 2017
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-	==~~NMEPHEB25 INSULIN ANALOGUE CRYSTAL STRUCTURE~~==	+	==NMePheB25 insulin analogue crystal structure==
	<StructureSection load='3zqr' size='340' side='right' caption='[[3zqr]], [[Resolution\|resolution]] 1.90Å' scene=''>		<StructureSection load='3zqr' size='340' side='right' caption='[[3zqr]], [[Resolution\|resolution]] 1.90Å' scene=''>
	== Structural highlights ==		== Structural highlights ==

OCA at 07:43, 5 August 2016

2016-08-05T07:43:20Z

←Older revision		Revision as of 07:43, 5 August 2016
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		+
	==NMEPHEB25 INSULIN ANALOGUE CRYSTAL STRUCTURE==		==NMEPHEB25 INSULIN ANALOGUE CRYSTAL STRUCTURE==
	<StructureSection load='3zqr' size='340' side='right' caption='[[3zqr]], [[Resolution\|resolution]] 1.90Å' scene=''>		<StructureSection load='3zqr' size='340' side='right' caption='[[3zqr]], [[Resolution\|resolution]] 1.90Å' scene=''>
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	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MEA:N-METHYLPHENYLALANINE'>MEA</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MEA:N-METHYLPHENYLALANINE'>MEA</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1hit\|1hit]], [[2hho\|2hho]], [[2c8q\|2c8q]], [[2w44\|2w44]], [[1tyl\|1tyl]], [[2c8r\|2c8r]], [[1t1k\|1t1k]], [[2wrv\|2wrv]], [[1aiy\|1aiy]], [[1xda\|1xda]], [[1htv\|1htv]], [[1mso\|1mso]], [[1uz9\|1uz9]], [[2ws6\|2ws6]], [[1fub\|1fub]], [[1tym\|1tym]], [[1hui\|1hui]], [[2vk0\|2vk0]], [[1vkt\|1vkt]], [[1hls\|1hls]], [[2ceu\|2ceu]], [[1t1q\|1t1q]], [[1qj0\|1qj0]], [[2ws0\|2ws0]], [[1mhj\|1mhj]], [[1fu2\|1fu2]], [[1sjt\|1sjt]], [[1qiy\|1qiy]], [[1iog\|1iog]], [[2vjz\|2vjz]], [[1ioh\|1ioh]], [[1trz\|1trz]], [[1evr\|1evr]], [[1sju\|1sju]], [[1ev3\|1ev3]], [[1rwe\|1rwe]], [[1os4\|1os4]], [[1guj\|1guj]], [[1ai0\|1ai0]], [[1sf1\|1sf1]], [[1jco\|1jco]], [[1jca\|1jca]], [[1zeg\|1zeg]], [[1os3\|1os3]], [[1xgl\|1xgl]], [[1qiz\|1qiz]], [[1t0c\|1t0c]], [[1g7b\|1g7b]], [[2wby\|2wby]], [[2aiy\|2aiy]], [[1ev6\|1ev6]], [[1q4v\|1q4v]], [[2ws7\|2ws7]], [[2hh4\|2hh4]], [[2h67\|2h67]], [[4aiy\|4aiy]], [[1j73\|1j73]], [[1k3m\|1k3m]], [[1mhi\|1mhi]], [[2wc0\|2wc0]], [[1kmf\|1kmf]], [[2hiu\|2hiu]], [[1xw7\|1xw7]], [[2wrw\|2wrw]], [[5aiy\|5aiy]], [[1g7a\|1g7a]], [[1znj\|1znj]], [[2ws4\|2ws4]], [[1zeh\|1zeh]], [[1his\|1his]], [[1b9e\|1b9e]], [[3aiy\|3aiy]], [[1w8p\|1w8p]], [[2ws1\|2ws1]], [[2wrx\|2wrx]], [[1hiq\|1hiq]], [[1lph\|1lph]], [[1efe\|1efe]], [[1a7f\|1a7f]], [[1t1p\|1t1p]], [[1ben\|1ben]], [[2wru\|2wru]], [[1lkq\|1lkq]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1hit\|1hit]], [[2hho\|2hho]], [[2c8q\|2c8q]], [[2w44\|2w44]], [[1tyl\|1tyl]], [[2c8r\|2c8r]], [[1t1k\|1t1k]], [[2wrv\|2wrv]], [[1aiy\|1aiy]], [[1xda\|1xda]], [[1htv\|1htv]], [[1mso\|1mso]], [[1uz9\|1uz9]], [[2ws6\|2ws6]], [[1fub\|1fub]], [[1tym\|1tym]], [[1hui\|1hui]], [[2vk0\|2vk0]], [[1vkt\|1vkt]], [[1hls\|1hls]], [[2ceu\|2ceu]], [[1t1q\|1t1q]], [[1qj0\|1qj0]], [[2ws0\|2ws0]], [[1mhj\|1mhj]], [[1fu2\|1fu2]], [[1sjt\|1sjt]], [[1qiy\|1qiy]], [[1iog\|1iog]], [[2vjz\|2vjz]], [[1ioh\|1ioh]], [[1trz\|1trz]], [[1evr\|1evr]], [[1sju\|1sju]], [[1ev3\|1ev3]], [[1rwe\|1rwe]], [[1os4\|1os4]], [[1guj\|1guj]], [[1ai0\|1ai0]], [[1sf1\|1sf1]], [[1jco\|1jco]], [[1jca\|1jca]], [[1zeg\|1zeg]], [[1os3\|1os3]], [[1xgl\|1xgl]], [[1qiz\|1qiz]], [[1t0c\|1t0c]], [[1g7b\|1g7b]], [[2wby\|2wby]], [[2aiy\|2aiy]], [[1ev6\|1ev6]], [[1q4v\|1q4v]], [[2ws7\|2ws7]], [[2hh4\|2hh4]], [[2h67\|2h67]], [[4aiy\|4aiy]], [[1j73\|1j73]], [[1k3m\|1k3m]], [[1mhi\|1mhi]], [[2wc0\|2wc0]], [[1kmf\|1kmf]], [[2hiu\|2hiu]], [[1xw7\|1xw7]], [[2wrw\|2wrw]], [[5aiy\|5aiy]], [[1g7a\|1g7a]], [[1znj\|1znj]], [[2ws4\|2ws4]], [[1zeh\|1zeh]], [[1his\|1his]], [[1b9e\|1b9e]], [[3aiy\|3aiy]], [[1w8p\|1w8p]], [[2ws1\|2ws1]], [[2wrx\|2wrx]], [[1hiq\|1hiq]], [[1lph\|1lph]], [[1efe\|1efe]], [[1a7f\|1a7f]], [[1t1p\|1t1p]], [[1ben\|1ben]], [[2wru\|2wru]], [[1lkq\|1lkq]]</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=3zqr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3zqr OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3zqr RCSB], [http://www.ebi.ac.uk/pdbsum/3zqr 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=3zqr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3zqr OCA], [http://pdbe.org/3zqr PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3zqr RCSB], [http://www.ebi.ac.uk/pdbsum/3zqr PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3zqr ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
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	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 3zqr" style="background-color:#fffaf0;"></div>

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

OCA at 10:02, 21 December 2014

2014-12-21T10:02:32Z

←Older revision		Revision as of 10:02, 21 December 2014
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-	~~{{STRUCTURE_3zqr~~\| ~~PDB~~=3zqr \| ~~SCENE~~= }}	+	==NMEPHEB25 INSULIN ANALOGUE CRYSTAL STRUCTURE==
-	===~~NMEPHEB25 INSULIN ANALOGUE CRYSTAL STRUCTURE~~===	+	<StructureSection load='3zqr' size='340' side='right' caption='[[3zqr]], [[Resolution\|resolution]] 1.90Å' scene=''>
-	~~{{ABSTRACT_PUBMED_21880708}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[3zqr]] is a 12 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3ZQR OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3ZQR FirstGlance]. <br>
		+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
		+	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MEA:N-METHYLPHENYLALANINE'>MEA</scene></td></tr>
		+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1hit\|1hit]], [[2hho\|2hho]], [[2c8q\|2c8q]], [[2w44\|2w44]], [[1tyl\|1tyl]], [[2c8r\|2c8r]], [[1t1k\|1t1k]], [[2wrv\|2wrv]], [[1aiy\|1aiy]], [[1xda\|1xda]], [[1htv\|1htv]], [[1mso\|1mso]], [[1uz9\|1uz9]], [[2ws6\|2ws6]], [[1fub\|1fub]], [[1tym\|1tym]], [[1hui\|1hui]], [[2vk0\|2vk0]], [[1vkt\|1vkt]], [[1hls\|1hls]], [[2ceu\|2ceu]], [[1t1q\|1t1q]], [[1qj0\|1qj0]], [[2ws0\|2ws0]], [[1mhj\|1mhj]], [[1fu2\|1fu2]], [[1sjt\|1sjt]], [[1qiy\|1qiy]], [[1iog\|1iog]], [[2vjz\|2vjz]], [[1ioh\|1ioh]], [[1trz\|1trz]], [[1evr\|1evr]], [[1sju\|1sju]], [[1ev3\|1ev3]], [[1rwe\|1rwe]], [[1os4\|1os4]], [[1guj\|1guj]], [[1ai0\|1ai0]], [[1sf1\|1sf1]], [[1jco\|1jco]], [[1jca\|1jca]], [[1zeg\|1zeg]], [[1os3\|1os3]], [[1xgl\|1xgl]], [[1qiz\|1qiz]], [[1t0c\|1t0c]], [[1g7b\|1g7b]], [[2wby\|2wby]], [[2aiy\|2aiy]], [[1ev6\|1ev6]], [[1q4v\|1q4v]], [[2ws7\|2ws7]], [[2hh4\|2hh4]], [[2h67\|2h67]], [[4aiy\|4aiy]], [[1j73\|1j73]], [[1k3m\|1k3m]], [[1mhi\|1mhi]], [[2wc0\|2wc0]], [[1kmf\|1kmf]], [[2hiu\|2hiu]], [[1xw7\|1xw7]], [[2wrw\|2wrw]], [[5aiy\|5aiy]], [[1g7a\|1g7a]], [[1znj\|1znj]], [[2ws4\|2ws4]], [[1zeh\|1zeh]], [[1his\|1his]], [[1b9e\|1b9e]], [[3aiy\|3aiy]], [[1w8p\|1w8p]], [[2ws1\|2ws1]], [[2wrx\|2wrx]], [[1hiq\|1hiq]], [[1lph\|1lph]], [[1efe\|1efe]], [[1a7f\|1a7f]], [[1t1p\|1t1p]], [[1ben\|1ben]], [[2wru\|2wru]], [[1lkq\|1lkq]]</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=3zqr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3zqr OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3zqr RCSB], [http://www.ebi.ac.uk/pdbsum/3zqr PDBsum]</span></td></tr>
		+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Defects in INS are the cause of familial hyperproinsulinemia (FHPRI) [MIM:[http://omim.org/entry/176730 176730]].<ref>PMID:3470784</ref> <ref>PMID:2196279</ref> <ref>PMID:4019786</ref> <ref>PMID:1601997</ref> Defects in INS are a cause of diabetes mellitus insulin-dependent type 2 (IDDM2) [MIM:[http://omim.org/entry/125852 125852]]. IDDM2 is a multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Clinical fetaures are polydipsia, polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.<ref>PMID:18192540</ref> Defects in INS are a cause of diabetes mellitus permanent neonatal (PNDM) [MIM:[http://omim.org/entry/606176 606176]]. PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy.<ref>PMID:17855560</ref> <ref>PMID:18162506</ref> Defects in INS are a cause of maturity-onset diabetes of the young type 10 (MODY10) [MIM:[http://omim.org/entry/613370 613370]]. MODY10 is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.<ref>PMID:18192540</ref> <ref>PMID:18162506</ref> <ref>PMID:20226046</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver.
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Apart from its role in insulin receptor (IR) activation, the C terminus of the B-chain of insulin is also responsible for the formation of insulin dimers. The dimerization of insulin plays an important role in the endogenous delivery of the hormone and in the administration of insulin to patients. Here, we investigated insulin analogues with selective N-methylations of peptide bond amides at positions B24, B25, or B26 to delineate their structural and functional contribution to the dimer interface. All N-methylated analogues showed impaired binding affinities to IR, which suggests a direct IR-interacting role for the respective amide hydrogens. The dimerization capabilities of analogues were investigated by isothermal microcalorimetry. Selective N-methylations of B24, B25, or B26 amides resulted in reduced dimerization abilities compared with native insulin (K(d) = 8.8 mum). Interestingly, although the N-methylation in [NMeTyrB26]-insulin or [NMePheB24]-insulin resulted in K(d) values of 142 and 587 mum, respectively, the [NMePheB25]-insulin did not form dimers even at high concentrations. This effect may be attributed to the loss of intramolecular hydrogen bonding between NHB25 and COA19, which connects the B-chain beta-strand to the core of the molecule. The release of the B-chain beta-strand from this hydrogen bond lock may result in its higher mobility, thereby shifting solution equilibrium toward the monomeric state of the hormone. The study was complemented by analyses of two novel analogue crystal structures. All examined analogues crystallized only in the most stable R(6) form of insulin oligomers (even if the dimer interface was totally disrupted), confirming the role of R(6)-specific intra/intermolecular interactions for hexamer stability.

-	~~==Disease==~~	+	Non-equivalent Role of Inter- and Intramolecular Hydrogen Bonds in the Insulin Dimer Interface.,Antolikova E, Zakova L, Turkenburg JP, Watson CJ, Hanclova I, Sanda M, Cooper A, Kraus T, Brzozowski AM, Jiracek J J Biol Chem. 2011 Oct 21;286(42):36968-77. Epub 2011 Aug 31. PMID:21880708<ref>PMID:21880708</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==~~	+
-	~~[[3zqr]] is a 12 chain structure~~. ~~Full crystallographic information is available from [http://oca~~.~~weizmann.ac.il~~/~~oca-bin/ocashort?id=3ZQR OCA].~~	+

	==See Also==		==See Also==
	*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]		*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:021880708</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
-	[[Category: Antolikova, E.]]	+	</StructureSection>
-	[[Category: Brzozowski, A M.]]	+	[[Category: Antolikova, E]]
-	[[Category: Cooper, A.]]	+	[[Category: Brzozowski, A M]]
-	[[Category: Hanclova, I.]]	+	[[Category: Cooper, A]]
-	[[Category: Jiracek, J A.]]	+	[[Category: Hanclova, I]]
-	[[Category: Kraus, T.]]	+	[[Category: Jiracek, J A]]
-	[[Category: Sanda, M.]]	+	[[Category: Kraus, T]]
-	[[Category: Turkenburg, J P.]]	+	[[Category: Sanda, M]]
-	[[Category: Watson, C J.]]	+	[[Category: Turkenburg, J P]]
-	[[Category: Zakova, L.]]	+	[[Category: Watson, C J]]
		+	[[Category: Zakova, L]]
	[[Category: Carbohydrate metabolism]]		[[Category: Carbohydrate metabolism]]
	[[Category: Diabetes mellitus]]		[[Category: Diabetes mellitus]]
	[[Category: Glucose metabolism]]		[[Category: Glucose metabolism]]
	[[Category: Hormone]]		[[Category: Hormone]]

OCA at 17:56, 24 March 2013

2013-03-24T17:56:14Z

←Older revision		Revision as of 17:56, 24 March 2013
Line 1:		Line 1:
-	[[Image:3zqr.png\|left\|200px]]
-
	{{STRUCTURE_3zqr\| PDB=3zqr \| SCENE= }}		{{STRUCTURE_3zqr\| PDB=3zqr \| SCENE= }}
-
	===NMEPHEB25 INSULIN ANALOGUE CRYSTAL STRUCTURE===		===NMEPHEB25 INSULIN ANALOGUE CRYSTAL STRUCTURE===
		+	{{ABSTRACT_PUBMED_21880708}}

-	~~{{ABSTRACT_PUBMED_21880708}}~~	+	==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:021880708</ref><references group="xtra"/>	+	<ref group="xtra">PMID:021880708</ref><references group="xtra"/><references/>
	[[Category: Antolikova, E.]]		[[Category: Antolikova, E.]]
	[[Category: Brzozowski, A M.]]		[[Category: Brzozowski, A M.]]

OCA at 19:11, 20 October 2012

2012-10-20T19:11:41Z

←Older revision		Revision as of 19:11, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[3zqr]] is a 12 chain structure ~~of [[Molecular Playground/Insulin]]~~. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3ZQR OCA].	+	[[3zqr]] is a 12 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3ZQR OCA].

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

OCA at 06:34, 27 July 2012

2012-07-27T06:34:59Z

←Older revision		Revision as of 06:34, 27 July 2012
Line 1:		Line 1:
	[[Image:3zqr.png\|left\|200px]]		[[Image:3zqr.png\|left\|200px]]

-	<!--
-	The line below this paragraph, containing "STRUCTURE_3zqr", 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_3zqr\| PDB=3zqr \| SCENE= }}		{{STRUCTURE_3zqr\| PDB=3zqr \| SCENE= }}

	===NMEPHEB25 INSULIN ANALOGUE CRYSTAL STRUCTURE===		===NMEPHEB25 INSULIN ANALOGUE CRYSTAL STRUCTURE===

-
-	<!--
-	The line below this paragraph, {{ABSTRACT_PUBMED_21880708}}, adds the Publication Abstract to the page
-	(as it appears on PubMed at http://www.pubmed.gov), where 21880708 is the PubMed ID number.
-	-->
	{{ABSTRACT_PUBMED_21880708}}		{{ABSTRACT_PUBMED_21880708}}

	==About this Structure==		==About this Structure==
-	[[3zqr]] is a 12 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3ZQR OCA].	+	[[3zqr]] is a 12 chain structure of [[Molecular Playground/Insulin]]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3ZQR OCA].
		+
		+	==See Also==
		+	*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]

	==Reference==		==Reference==

←Older revision		Revision as of 07:10, 18 August 2022
Line 3:		Line 3:
	<StructureSection load='3zqr' size='340' side='right'caption='[[3zqr]], [[Resolution\|resolution]] 1.90Å' scene=''>		<StructureSection load='3zqr' size='340' side='right'caption='[[3zqr]], [[Resolution\|resolution]] 1.90Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3zqr]] is a 12 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3ZQR OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3ZQR FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3zqr]] is a 12 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3ZQR OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3ZQR FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=IPH:PHENOL'>IPH</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MEA:N-METHYLPHENYLALANINE'>MEA</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=MEA:N-METHYLPHENYLALANINE'>MEA</scene></td></tr>
-	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1hit\|1hit]], [[2hho\|2hho]], [[2c8q\|2c8q]], [[2w44\|2w44]], [[1tyl\|1tyl]], [[2c8r\|2c8r]], [[1t1k\|1t1k]], [[2wrv\|2wrv]], [[1aiy\|1aiy]], [[1xda\|1xda]], [[1htv\|1htv]], [[1mso\|1mso]], [[1uz9\|1uz9]], [[2ws6\|2ws6]], [[1fub\|1fub]], [[1tym\|1tym]], [[1hui\|1hui]], [[2vk0\|2vk0]], [[1vkt\|1vkt]], [[1hls\|1hls]], [[2ceu\|2ceu]], [[1t1q\|1t1q]], [[1qj0\|1qj0]], [[2ws0\|2ws0]], [[1mhj\|1mhj]], [[1fu2\|1fu2]], [[1sjt\|1sjt]], [[1qiy\|1qiy]], [[1iog\|1iog]], [[2vjz\|2vjz]], [[1ioh\|1ioh]], [[1trz\|1trz]], [[1evr\|1evr]], [[1sju\|1sju]], [[1ev3\|1ev3]], [[1rwe\|1rwe]], [[1os4\|1os4]], [[1guj\|1guj]], [[1ai0\|1ai0]], [[1sf1\|1sf1]], [[1jco\|1jco]], [[1jca\|1jca]], [[1zeg\|1zeg]], [[1os3\|1os3]], [[1xgl\|1xgl]], [[1qiz\|1qiz]], [[1t0c\|1t0c]], [[1g7b\|1g7b]], [[2wby\|2wby]], [[2aiy\|2aiy]], [[1ev6\|1ev6]], [[1q4v\|1q4v]], [[2ws7\|2ws7]], [[2hh4\|2hh4]], [[2h67\|2h67]], [[4aiy\|4aiy]], [[1j73\|1j73]], [[1k3m\|1k3m]], [[1mhi\|1mhi]], [[2wc0\|2wc0]], [[1kmf\|1kmf]], [[2hiu\|2hiu]], [[1xw7\|1xw7]], [[2wrw\|2wrw]], [[5aiy\|5aiy]], [[1g7a\|1g7a]], [[1znj\|1znj]], [[2ws4\|2ws4]], [[1zeh\|1zeh]], [[1his\|1his]], [[1b9e\|1b9e]], [[3aiy\|3aiy]], [[1w8p\|1w8p]], [[2ws1\|2ws1]], [[2wrx\|2wrx]], [[1hiq\|1hiq]], [[1lph\|1lph]], [[1efe\|1efe]], [[1a7f\|1a7f]], [[1t1p\|1t1p]], [[1ben\|1ben]], [[2wru\|2wru]], [[1lkq\|1lkq]]</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]], [[2w44\|2w44]], [[1tyl\|1tyl]], [[2c8r\|2c8r]], [[1t1k\|1t1k]], [[2wrv\|2wrv]], [[1aiy\|1aiy]], [[1xda\|1xda]], [[1htv\|1htv]], [[1mso\|1mso]], [[1uz9\|1uz9]], [[2ws6\|2ws6]], [[1fub\|1fub]], [[1tym\|1tym]], [[1hui\|1hui]], [[2vk0\|2vk0]], [[1vkt\|1vkt]], [[1hls\|1hls]], [[2ceu\|2ceu]], [[1t1q\|1t1q]], [[1qj0\|1qj0]], [[2ws0\|2ws0]], [[1mhj\|1mhj]], [[1fu2\|1fu2]], [[1sjt\|1sjt]], [[1qiy\|1qiy]], [[1iog\|1iog]], [[2vjz\|2vjz]], [[1ioh\|1ioh]], [[1trz\|1trz]], [[1evr\|1evr]], [[1sju\|1sju]], [[1ev3\|1ev3]], [[1rwe\|1rwe]], [[1os4\|1os4]], [[1guj\|1guj]], [[1ai0\|1ai0]], [[1sf1\|1sf1]], [[1jco\|1jco]], [[1jca\|1jca]], [[1zeg\|1zeg]], [[1os3\|1os3]], [[1xgl\|1xgl]], [[1qiz\|1qiz]], [[1t0c\|1t0c]], [[1g7b\|1g7b]], [[2wby\|2wby]], [[2aiy\|2aiy]], [[1ev6\|1ev6]], [[1q4v\|1q4v]], [[2ws7\|2ws7]], [[2hh4\|2hh4]], [[2h67\|2h67]], [[4aiy\|4aiy]], [[1j73\|1j73]], [[1k3m\|1k3m]], [[1mhi\|1mhi]], [[2wc0\|2wc0]], [[1kmf\|1kmf]], [[2hiu\|2hiu]], [[1xw7\|1xw7]], [[2wrw\|2wrw]], [[5aiy\|5aiy]], [[1g7a\|1g7a]], [[1znj\|1znj]], [[2ws4\|2ws4]], [[1zeh\|1zeh]], [[1his\|1his]], [[1b9e\|1b9e]], [[3aiy\|3aiy]], [[1w8p\|1w8p]], [[2ws1\|2ws1]], [[2wrx\|2wrx]], [[1hiq\|1hiq]], [[1lph\|1lph]], [[1efe\|1efe]], [[1a7f\|1a7f]], [[1t1p\|1t1p]], [[1ben\|1ben]], [[2wru\|2wru]], [[1lkq\|1lkq]]</div></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=3zqr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3zqr OCA], [~~http~~://pdbe.org/3zqr PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3zqr RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3zqr PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3zqr 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=3zqr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3zqr OCA], [https://pdbe.org/3zqr PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3zqr RCSB], [https://www.ebi.ac.uk/pdbsum/3zqr PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3zqr ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Defects in INS are the cause of familial hyperproinsulinemia (FHPRI) [MIM:[~~http~~://omim.org/entry/176730 176730]].<ref>PMID:3470784</ref> <ref>PMID:2196279</ref> <ref>PMID:4019786</ref> <ref>PMID:1601997</ref> Defects in INS are a cause of diabetes mellitus insulin-dependent type 2 (IDDM2) [MIM:[~~http~~://omim.org/entry/125852 125852]]. IDDM2 is a multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Clinical fetaures are polydipsia, polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.<ref>PMID:18192540</ref> Defects in INS are a cause of diabetes mellitus permanent neonatal (PNDM) [MIM:[~~http~~://omim.org/entry/606176 606176]]. PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy.<ref>PMID:17855560</ref> <ref>PMID:18162506</ref> Defects in INS are a cause of maturity-onset diabetes of the young type 10 (MODY10) [MIM:[~~http~~://omim.org/entry/613370 613370]]. MODY10 is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.<ref>PMID:18192540</ref> <ref>PMID:18162506</ref> <ref>PMID:20226046</ref>	+	[[https://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Defects in INS are the cause of familial hyperproinsulinemia (FHPRI) [MIM:[https://omim.org/entry/176730 176730]].<ref>PMID:3470784</ref> <ref>PMID:2196279</ref> <ref>PMID:4019786</ref> <ref>PMID:1601997</ref> Defects in INS are a cause of diabetes mellitus insulin-dependent type 2 (IDDM2) [MIM:[https://omim.org/entry/125852 125852]]. IDDM2 is a multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Clinical fetaures are polydipsia, polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.<ref>PMID:18192540</ref> Defects in INS are a cause of diabetes mellitus permanent neonatal (PNDM) [MIM:[https://omim.org/entry/606176 606176]]. PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy.<ref>PMID:17855560</ref> <ref>PMID:18162506</ref> Defects in INS are a cause of maturity-onset diabetes of the young type 10 (MODY10) [MIM:[https://omim.org/entry/613370 613370]]. MODY10 is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.<ref>PMID:18192540</ref> <ref>PMID:18162506</ref> <ref>PMID:20226046</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver.	+	[[https://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN]] Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver.
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==