1guj - Revision history

OCA at 12:07, 13 December 2023

OCA — Wed, 13 Dec 2023 12:07:00 GMT

←Older revision		Revision as of 12:07, 13 December 2023
Line 3:		Line 3:
	<StructureSection load='1guj' size='340' side='right'caption='[[1guj]], [[Resolution\|resolution]] 1.62Å' scene=''>		<StructureSection load='1guj' size='340' side='right'caption='[[1guj]], [[Resolution\|resolution]] 1.62Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1guj]] is a 4 chain structure with sequence from [https://en.wikipedia.org/wiki/~~Human Human~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1GUJ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1GUJ FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1guj]] 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=1GUJ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1GUJ FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene>~~</td></tr>	+	</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution\|Resolution]] 1.62Å</td></tr>
-	<tr id='~~related~~'><td class="sblockLbl"><b>[[~~Related_structure~~\|~~Related~~:]]</b></td><td class="sblockDat"><~~div style~~='~~overflow~~: ~~auto; max-height: 3em;~~'>[[1a7f\|1a7f]], [[1ai0\|1ai0]], [[1aiy\|1aiy]], [[1b9e\|1b9e]], [[1ben\|1ben]], [[1hiq\|1hiq]], [[1his\|1his]], [[1hit\|1hit]], [[1hls\|1hls]], [[1htv\|1htv]], [[1hui\|1hui]], [[1iog\|1iog]], [[1ioh\|1ioh]], [[1j73\|1j73]], [[1jca\|1jca]], [[1jco\|1jco]], [[1k3m\|1k3m]], [[1lph\|1lph]], [[1mhi\|1mhi]], [[1mhj\|1mhj]], [[1qiy\|1qiy]], [[1qiz\|1qiz]], [[1qj0\|1qj0]], [[1sjt\|1sjt]], [[1sju\|1sju]], [[1trz\|1trz]], [[1tyl\|1tyl]], [[1tym\|1tym]], [[1vks\|1vks]], [[1vkt\|1vkt]], [[1xda\|1xda]], [[1xgl\|1xgl]], [[1zeg\|1zeg]], [[1zeh\|1zeh]], [[1znj\|1znj]], [[2aiy\|2aiy]], [[2hiu\|2hiu]], [[3aiy\|3aiy]], [[4aiy\|4aiy]], [[5aiy\|5aiy]]</~~div~~></td></tr>	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=1guj FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1guj OCA], [https://pdbe.org/1guj PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1guj RCSB], [https://www.ebi.ac.uk/pdbsum/1guj PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1guj 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=1guj FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1guj OCA], [https://pdbe.org/1guj PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1guj RCSB], [https://www.ebi.ac.uk/pdbsum/1guj PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1guj 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: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Brange, J]]	+	[[Category: Brange J]]
-	[[Category: Chance, K]]	+	[[Category: Chance K]]
-	[[Category: Dodson~~, G G~~]]	+	[[Category: Dodson GG]]
-	[[Category: Finch, J]]	+	[[Category: Finch J]]
-	[[Category: Scott~~, D J~~]]	+	[[Category: Scott DJ]]
-	[[Category: Whittingham~~, J L~~]]	+	[[Category: Whittingham JL]]
-	[[Category: Wilson, A]]	+	[[Category: Wilson A]]
-	~~[[Category: Hormone]]~~	+
-	~~[[Category: Low ph]]~~	+
-	~~[[Category: Metabolic role]]~~	+
-	~~[[Category: Sulphate ion~~]]	+

OCA at 10:24, 17 February 2021

OCA — Wed, 17 Feb 2021 10:24:42 GMT

←Older revision		Revision as of 10:24, 17 February 2021
Line 3:		Line 3:
	<StructureSection load='1guj' size='340' side='right'caption='[[1guj]], [[Resolution\|resolution]] 1.62Å' scene=''>		<StructureSection load='1guj' size='340' side='right'caption='[[1guj]], [[Resolution\|resolution]] 1.62Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1guj]] is a 4 chain structure with sequence from [~~http~~://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1GUJ OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=1GUJ FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1guj]] is a 4 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1GUJ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1GUJ FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
-	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1a7f\|1a7f]], [[1ai0\|1ai0]], [[1aiy\|1aiy]], [[1b9e\|1b9e]], [[1ben\|1ben]], [[1hiq\|1hiq]], [[1his\|1his]], [[1hit\|1hit]], [[1hls\|1hls]], [[1htv\|1htv]], [[1hui\|1hui]], [[1iog\|1iog]], [[1ioh\|1ioh]], [[1j73\|1j73]], [[1jca\|1jca]], [[1jco\|1jco]], [[1k3m\|1k3m]], [[1lph\|1lph]], [[1mhi\|1mhi]], [[1mhj\|1mhj]], [[1qiy\|1qiy]], [[1qiz\|1qiz]], [[1qj0\|1qj0]], [[1sjt\|1sjt]], [[1sju\|1sju]], [[1trz\|1trz]], [[1tyl\|1tyl]], [[1tym\|1tym]], [[1vks\|1vks]], [[1vkt\|1vkt]], [[1xda\|1xda]], [[1xgl\|1xgl]], [[1zeg\|1zeg]], [[1zeh\|1zeh]], [[1znj\|1znj]], [[2aiy\|2aiy]], [[2hiu\|2hiu]], [[3aiy\|3aiy]], [[4aiy\|4aiy]], [[5aiy\|5aiy]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[1a7f\|1a7f]], [[1ai0\|1ai0]], [[1aiy\|1aiy]], [[1b9e\|1b9e]], [[1ben\|1ben]], [[1hiq\|1hiq]], [[1his\|1his]], [[1hit\|1hit]], [[1hls\|1hls]], [[1htv\|1htv]], [[1hui\|1hui]], [[1iog\|1iog]], [[1ioh\|1ioh]], [[1j73\|1j73]], [[1jca\|1jca]], [[1jco\|1jco]], [[1k3m\|1k3m]], [[1lph\|1lph]], [[1mhi\|1mhi]], [[1mhj\|1mhj]], [[1qiy\|1qiy]], [[1qiz\|1qiz]], [[1qj0\|1qj0]], [[1sjt\|1sjt]], [[1sju\|1sju]], [[1trz\|1trz]], [[1tyl\|1tyl]], [[1tym\|1tym]], [[1vks\|1vks]], [[1vkt\|1vkt]], [[1xda\|1xda]], [[1xgl\|1xgl]], [[1zeg\|1zeg]], [[1zeh\|1zeh]], [[1znj\|1znj]], [[2aiy\|2aiy]], [[2hiu\|2hiu]], [[3aiy\|3aiy]], [[4aiy\|4aiy]], [[5aiy\|5aiy]]</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=1guj FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1guj OCA], [~~http~~://pdbe.org/1guj PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=1guj RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/1guj PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=1guj 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=1guj FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1guj OCA], [https://pdbe.org/1guj PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1guj RCSB], [https://www.ebi.ac.uk/pdbsum/1guj PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1guj 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]]
Line 33:		Line 33:

	==See Also==		==See Also==
-	*[[~~Molecular Playground/~~Insulin\|~~Molecular Playground/~~Insulin]]	+	*[[Insulin 3D Structures\|Insulin 3D Structures]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 11:34, 10 May 2019

OCA — Fri, 10 May 2019 11:34:33 GMT

←Older revision		Revision as of 11:34, 10 May 2019
Line 1:		Line 1:

	==Insulin at pH 2: structural analysis of the conditions promoting insulin fibre formation.==		==Insulin at pH 2: structural analysis of the conditions promoting insulin fibre formation.==
-	<StructureSection load='1guj' size='340' side='right' caption='[[1guj]], [[Resolution\|resolution]] 1.62Å' scene=''>	+	<StructureSection load='1guj' size='340' side='right'caption='[[1guj]], [[Resolution\|resolution]] 1.62Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[1guj]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1GUJ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1GUJ FirstGlance]. <br>		<table><tr><td colspan='2'>[[1guj]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1GUJ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1GUJ FirstGlance]. <br>
Line 31:		Line 31:
	</div>		</div>
	<div class="pdbe-citations 1guj" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 1guj" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]
	== References ==		== References ==
	<references/>		<references/>
Line 36:		Line 39:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Brange, J]]		[[Category: Brange, J]]
	[[Category: Chance, K]]		[[Category: Chance, K]]

OCA at 06:36, 3 January 2018

OCA — Wed, 03 Jan 2018 06:36:58 GMT

←Older revision		Revision as of 06:36, 3 January 2018
Line 1:		Line 1:
-	==~~INSULIN AT PH~~ 2: ~~STRUCTURAL ANALYSIS OF THE CONDITIONS PROMOTING INSULIN FIBRE FORMATION~~.==	+
		+	==Insulin at pH 2: structural analysis of the conditions promoting insulin fibre formation.==
	<StructureSection load='1guj' size='340' side='right' caption='[[1guj]], [[Resolution\|resolution]] 1.62Å' scene=''>		<StructureSection load='1guj' size='340' side='right' caption='[[1guj]], [[Resolution\|resolution]] 1.62Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
Line 5:		Line 6:
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1a7f\|1a7f]], [[1ai0\|1ai0]], [[1aiy\|1aiy]], [[1b9e\|1b9e]], [[1ben\|1ben]], [[1hiq\|1hiq]], [[1his\|1his]], [[1hit\|1hit]], [[1hls\|1hls]], [[1htv\|1htv]], [[1hui\|1hui]], [[1iog\|1iog]], [[1ioh\|1ioh]], [[1j73\|1j73]], [[1jca\|1jca]], [[1jco\|1jco]], [[1k3m\|1k3m]], [[1lph\|1lph]], [[1mhi\|1mhi]], [[1mhj\|1mhj]], [[1qiy\|1qiy]], [[1qiz\|1qiz]], [[1qj0\|1qj0]], [[1sjt\|1sjt]], [[1sju\|1sju]], [[1trz\|1trz]], [[1tyl\|1tyl]], [[1tym\|1tym]], [[1vks\|1vks]], [[1vkt\|1vkt]], [[1xda\|1xda]], [[1xgl\|1xgl]], [[1zeg\|1zeg]], [[1zeh\|1zeh]], [[1znj\|1znj]], [[2aiy\|2aiy]], [[2hiu\|2hiu]], [[3aiy\|3aiy]], [[4aiy\|4aiy]], [[5aiy\|5aiy]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1a7f\|1a7f]], [[1ai0\|1ai0]], [[1aiy\|1aiy]], [[1b9e\|1b9e]], [[1ben\|1ben]], [[1hiq\|1hiq]], [[1his\|1his]], [[1hit\|1hit]], [[1hls\|1hls]], [[1htv\|1htv]], [[1hui\|1hui]], [[1iog\|1iog]], [[1ioh\|1ioh]], [[1j73\|1j73]], [[1jca\|1jca]], [[1jco\|1jco]], [[1k3m\|1k3m]], [[1lph\|1lph]], [[1mhi\|1mhi]], [[1mhj\|1mhj]], [[1qiy\|1qiy]], [[1qiz\|1qiz]], [[1qj0\|1qj0]], [[1sjt\|1sjt]], [[1sju\|1sju]], [[1trz\|1trz]], [[1tyl\|1tyl]], [[1tym\|1tym]], [[1vks\|1vks]], [[1vkt\|1vkt]], [[1xda\|1xda]], [[1xgl\|1xgl]], [[1zeg\|1zeg]], [[1zeh\|1zeh]], [[1znj\|1znj]], [[2aiy\|2aiy]], [[2hiu\|2hiu]], [[3aiy\|3aiy]], [[4aiy\|4aiy]], [[5aiy\|5aiy]]</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=1guj FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1guj OCA], [http://pdbe.org/1guj PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1guj RCSB], [http://www.ebi.ac.uk/pdbsum/1guj 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=1guj FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1guj OCA], [http://pdbe.org/1guj PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1guj RCSB], [http://www.ebi.ac.uk/pdbsum/1guj PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=1guj ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 15:		Line 16:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/gu/1guj_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/gu/1guj_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>
Line 30:		Line 31:
	</div>		</div>
	<div class="pdbe-citations 1guj" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 1guj" style="background-color:#fffaf0;"></div>
-
-	==See Also==
-	*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 15:19, 9 February 2016

OCA — Tue, 09 Feb 2016 15:19:57 GMT

←Older revision		Revision as of 15:19, 9 February 2016
Line 19:		Line 19:
	<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=1guj ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">

OCA at 23:31, 10 September 2015

OCA — Thu, 10 Sep 2015 23:31:15 GMT

←Older revision		Revision as of 23:31, 10 September 2015
Line 2:		Line 2:
	<StructureSection load='1guj' size='340' side='right' caption='[[1guj]], [[Resolution\|resolution]] 1.62Å' scene=''>		<StructureSection load='1guj' size='340' side='right' caption='[[1guj]], [[Resolution\|resolution]] 1.62Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1guj]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/~~Homo_sapiens Homo sapiens~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1GUJ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1GUJ FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1guj]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1GUJ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1GUJ FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1a7f\|1a7f]], [[1ai0\|1ai0]], [[1aiy\|1aiy]], [[1b9e\|1b9e]], [[1ben\|1ben]], [[1hiq\|1hiq]], [[1his\|1his]], [[1hit\|1hit]], [[1hls\|1hls]], [[1htv\|1htv]], [[1hui\|1hui]], [[1iog\|1iog]], [[1ioh\|1ioh]], [[1j73\|1j73]], [[1jca\|1jca]], [[1jco\|1jco]], [[1k3m\|1k3m]], [[1lph\|1lph]], [[1mhi\|1mhi]], [[1mhj\|1mhj]], [[1qiy\|1qiy]], [[1qiz\|1qiz]], [[1qj0\|1qj0]], [[1sjt\|1sjt]], [[1sju\|1sju]], [[1trz\|1trz]], [[1tyl\|1tyl]], [[1tym\|1tym]], [[1vks\|1vks]], [[1vkt\|1vkt]], [[1xda\|1xda]], [[1xgl\|1xgl]], [[1zeg\|1zeg]], [[1zeh\|1zeh]], [[1znj\|1znj]], [[2aiy\|2aiy]], [[2hiu\|2hiu]], [[3aiy\|3aiy]], [[4aiy\|4aiy]], [[5aiy\|5aiy]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1a7f\|1a7f]], [[1ai0\|1ai0]], [[1aiy\|1aiy]], [[1b9e\|1b9e]], [[1ben\|1ben]], [[1hiq\|1hiq]], [[1his\|1his]], [[1hit\|1hit]], [[1hls\|1hls]], [[1htv\|1htv]], [[1hui\|1hui]], [[1iog\|1iog]], [[1ioh\|1ioh]], [[1j73\|1j73]], [[1jca\|1jca]], [[1jco\|1jco]], [[1k3m\|1k3m]], [[1lph\|1lph]], [[1mhi\|1mhi]], [[1mhj\|1mhj]], [[1qiy\|1qiy]], [[1qiz\|1qiz]], [[1qj0\|1qj0]], [[1sjt\|1sjt]], [[1sju\|1sju]], [[1trz\|1trz]], [[1tyl\|1tyl]], [[1tym\|1tym]], [[1vks\|1vks]], [[1vkt\|1vkt]], [[1xda\|1xda]], [[1xgl\|1xgl]], [[1zeg\|1zeg]], [[1zeh\|1zeh]], [[1znj\|1znj]], [[2aiy\|2aiy]], [[2hiu\|2hiu]], [[3aiy\|3aiy]], [[4aiy\|4aiy]], [[5aiy\|5aiy]]</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=1guj FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1guj OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1guj RCSB], [http://www.ebi.ac.uk/pdbsum/1guj 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=1guj FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1guj OCA], [http://pdbe.org/1guj PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1guj RCSB], [http://www.ebi.ac.uk/pdbsum/1guj PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 29:		Line 29:
	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 1guj" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 36:		Line 37:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Brange, J]]		[[Category: Brange, J]]
	[[Category: Chance, K]]		[[Category: Chance, K]]

OCA at 19:37, 22 December 2014

OCA — Mon, 22 Dec 2014 19:37:44 GMT

←Older revision		Revision as of 19:37, 22 December 2014
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[1guj]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1GUJ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1GUJ FirstGlance]. <br>		<table><tr><td colspan='2'>[[1guj]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1GUJ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1GUJ FirstGlance]. <br>
-	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene><br>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
-	<tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1a7f\|1a7f]], [[1ai0\|1ai0]], [[1aiy\|1aiy]], [[1b9e\|1b9e]], [[1ben\|1ben]], [[1hiq\|1hiq]], [[1his\|1his]], [[1hit\|1hit]], [[1hls\|1hls]], [[1htv\|1htv]], [[1hui\|1hui]], [[1iog\|1iog]], [[1ioh\|1ioh]], [[1j73\|1j73]], [[1jca\|1jca]], [[1jco\|1jco]], [[1k3m\|1k3m]], [[1lph\|1lph]], [[1mhi\|1mhi]], [[1mhj\|1mhj]], [[1qiy\|1qiy]], [[1qiz\|1qiz]], [[1qj0\|1qj0]], [[1sjt\|1sjt]], [[1sju\|1sju]], [[1trz\|1trz]], [[1tyl\|1tyl]], [[1tym\|1tym]], [[1vks\|1vks]], [[1vkt\|1vkt]], [[1xda\|1xda]], [[1xgl\|1xgl]], [[1zeg\|1zeg]], [[1zeh\|1zeh]], [[1znj\|1znj]], [[2aiy\|2aiy]], [[2hiu\|2hiu]], [[3aiy\|3aiy]], [[4aiy\|4aiy]], [[5aiy\|5aiy]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1a7f\|1a7f]], [[1ai0\|1ai0]], [[1aiy\|1aiy]], [[1b9e\|1b9e]], [[1ben\|1ben]], [[1hiq\|1hiq]], [[1his\|1his]], [[1hit\|1hit]], [[1hls\|1hls]], [[1htv\|1htv]], [[1hui\|1hui]], [[1iog\|1iog]], [[1ioh\|1ioh]], [[1j73\|1j73]], [[1jca\|1jca]], [[1jco\|1jco]], [[1k3m\|1k3m]], [[1lph\|1lph]], [[1mhi\|1mhi]], [[1mhj\|1mhj]], [[1qiy\|1qiy]], [[1qiz\|1qiz]], [[1qj0\|1qj0]], [[1sjt\|1sjt]], [[1sju\|1sju]], [[1trz\|1trz]], [[1tyl\|1tyl]], [[1tym\|1tym]], [[1vks\|1vks]], [[1vkt\|1vkt]], [[1xda\|1xda]], [[1xgl\|1xgl]], [[1zeg\|1zeg]], [[1zeh\|1zeh]], [[1znj\|1znj]], [[2aiy\|2aiy]], [[2hiu\|2hiu]], [[3aiy\|3aiy]], [[4aiy\|4aiy]], [[5aiy\|5aiy]]</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=1guj FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1guj OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1guj RCSB], [http://www.ebi.ac.uk/pdbsum/1guj 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=1guj FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1guj OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1guj RCSB], [http://www.ebi.ac.uk/pdbsum/1guj 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:
	</StructureSection>		</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Brange, J.]]	+	[[Category: Brange, J]]
-	[[Category: Chance, K.]]	+	[[Category: Chance, K]]
-	[[Category: Dodson, G G.]]	+	[[Category: Dodson, G G]]
-	[[Category: Finch, J.]]	+	[[Category: Finch, J]]
-	[[Category: Scott, D J.]]	+	[[Category: Scott, D J]]
-	[[Category: Whittingham, J L.]]	+	[[Category: Whittingham, J L]]
-	[[Category: Wilson, A.]]	+	[[Category: Wilson, A]]
	[[Category: Hormone]]		[[Category: Hormone]]
	[[Category: Low ph]]		[[Category: Low ph]]
	[[Category: Metabolic role]]		[[Category: Metabolic role]]
	[[Category: Sulphate ion]]		[[Category: Sulphate ion]]

OCA at 14:39, 29 September 2014

OCA — Mon, 29 Sep 2014 14:39:43 GMT

←Older revision		Revision as of 14:39, 29 September 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_1guj\| PDB=1guj \| SCENE= }}~~	+	==INSULIN AT PH 2: STRUCTURAL ANALYSIS OF THE CONDITIONS PROMOTING INSULIN FIBRE FORMATION.==
-	===INSULIN AT PH 2: STRUCTURAL ANALYSIS OF THE CONDITIONS PROMOTING INSULIN FIBRE FORMATION.===	+	<StructureSection load='1guj' size='340' side='right' caption='[[1guj]], [[Resolution\|resolution]] 1.62Å' scene=''>
-	~~{{ABSTRACT_PUBMED_12051853}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[1guj]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1GUJ OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1GUJ FirstGlance]. <br>
		+	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene><br>
		+	<tr><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1a7f\|1a7f]], [[1ai0\|1ai0]], [[1aiy\|1aiy]], [[1b9e\|1b9e]], [[1ben\|1ben]], [[1hiq\|1hiq]], [[1his\|1his]], [[1hit\|1hit]], [[1hls\|1hls]], [[1htv\|1htv]], [[1hui\|1hui]], [[1iog\|1iog]], [[1ioh\|1ioh]], [[1j73\|1j73]], [[1jca\|1jca]], [[1jco\|1jco]], [[1k3m\|1k3m]], [[1lph\|1lph]], [[1mhi\|1mhi]], [[1mhj\|1mhj]], [[1qiy\|1qiy]], [[1qiz\|1qiz]], [[1qj0\|1qj0]], [[1sjt\|1sjt]], [[1sju\|1sju]], [[1trz\|1trz]], [[1tyl\|1tyl]], [[1tym\|1tym]], [[1vks\|1vks]], [[1vkt\|1vkt]], [[1xda\|1xda]], [[1xgl\|1xgl]], [[1zeg\|1zeg]], [[1zeh\|1zeh]], [[1znj\|1znj]], [[2aiy\|2aiy]], [[2hiu\|2hiu]], [[3aiy\|3aiy]], [[4aiy\|4aiy]], [[5aiy\|5aiy]]</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=1guj FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1guj OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1guj RCSB], [http://www.ebi.ac.uk/pdbsum/1guj 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/gu/1guj_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 ==
		+	When insulin solutions are subjected to acid, heat and agitation, the normal pattern of insulin assembly (dimers-->tetramers-->hexamers) is disrupted; the molecule undergoes conformational changes allowing it to follow an alternative aggregation pathway (via a monomeric species) leading to the formation of insoluble amyloid fibres. To investigate the effect of acid pH on the conformation and aggregation state of the protein, the crystal structure of human insulin at pH 2.1 has been determined to 1.6 A resolution. The structure reveals that the native fold is maintained at low pH, and that the molecule is still capable of forming dimers similar to those found in hexameric insulin structures at higher pH. Sulphate ions are incorporated into the molecule and the crystal lattice where they neutralise positive charges on the protein, stabilising its structure and facilitating crystallisation. The sulphate interactions are associated with local deformations in the protein, which may indicate that the structure is more plastic at low pH. Transmission electron microscopy analysis of insulin fibres reveals that the appearance of the fibres is greatly influenced by the type of acid employed. Sulphuric acid produces distinctive highly bunched, truncated fibres, suggesting that the sulphate ions have a sophisticated role to play in fibre formation, rather as they do in the crystal structure. Analytical ultracentrifugation studies show that in the absence of heating, insulin is predominantly dimeric in mineral acids, whereas in acetic acid the equilibrium is shifted towards the monomer. Hence, the effect of acid on the aggregation state of insulin is also complex. These results suggest that acid conditions increase the susceptibility of the molecule to conformational change and dissociation, and enhance the rate of fibrillation by providing a charged environment in which the attractive forces between the protein molecules is increased.

-	~~==Disease==~~	+	Insulin at pH 2: structural analysis of the conditions promoting insulin fibre formation.,Whittingham JL, Scott DJ, Chance K, Wilson A, Finch J, Brange J, Guy Dodson G J Mol Biol. 2002 Apr 26;318(2):479-90. PMID:12051853<ref>PMID:12051853</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==~~	+
-	~~[[1guj]] is a 4 chain structure with sequence from [http://en~~.~~wikipedia~~.~~org~~/~~wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1GUJ OCA].~~	+

	==See Also==		==See Also==
	*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]		*[[Molecular Playground/Insulin\|Molecular Playground/Insulin]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:012051853</ref><ref group="xtra">PMID:010489447</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Brange, J.]]		[[Category: Brange, J.]]

OCA at 11:21, 24 March 2013

OCA — Sun, 24 Mar 2013 11:21:22 GMT

←Older revision		Revision as of 11:21, 24 March 2013
Line 1:		Line 1:
-	[[Image:1guj.png\|left\|200px]]
-
	{{STRUCTURE_1guj\| PDB=1guj \| SCENE= }}		{{STRUCTURE_1guj\| PDB=1guj \| SCENE= }}
-
	===INSULIN AT PH 2: STRUCTURAL ANALYSIS OF THE CONDITIONS PROMOTING INSULIN FIBRE FORMATION.===		===INSULIN AT PH 2: STRUCTURAL ANALYSIS OF THE CONDITIONS PROMOTING INSULIN FIBRE FORMATION.===
		+	{{ABSTRACT_PUBMED_12051853}}

-	~~{{ABSTRACT_PUBMED_12051853}}~~	+	==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:012051853</ref><ref group="xtra">PMID:010489447</ref><references group="xtra"/>	+	<ref group="xtra">PMID:012051853</ref><ref group="xtra">PMID:010489447</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Brange, J.]]		[[Category: Brange, J.]]

OCA at 14:17, 20 October 2012

OCA — Sat, 20 Oct 2012 14:17:30 GMT

←Older revision		Revision as of 14:17, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[1guj]] is a 4 chain structure ~~of [[Molecular Playground/Insulin]]~~ with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1GUJ OCA].	+	[[1guj]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1GUJ OCA].

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