3fgu - Revision history

OCA at 15:29, 1 November 2023

2023-11-01T15:29:34Z

←Older revision		Revision as of 15:29, 1 November 2023
Line 3:		Line 3:
	<StructureSection load='3fgu' size='340' side='right'caption='[[3fgu]], [[Resolution\|resolution]] 2.15Å' scene=''>		<StructureSection load='3fgu' size='340' side='right'caption='[[3fgu]], [[Resolution\|resolution]] 2.15Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3fgu]] is a 1 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=3FGU OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://proteopedia.org/fgij/fg.htm?mol=3FGU FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3fgu]] is a 1 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=3FGU OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3FGU FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=ANP:PHOSPHOAMINOPHOSPHONIC+ACID-ADENYLATE+ESTER'>ANP</scene>, <scene name='pdbligand=BGC:BETA-D-GLUCOSE'>BGC</scene>, <scene name='pdbligand=K:POTASSIUM+ION'>K</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</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]] 2.15Å</td></tr>
-	~~<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1v4s\|1v4s]], [[3f9m\|3f9m]], [[1v4t\|1v4t]]</td></tr>~~	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=ANP:PHOSPHOAMINOPHOSPHONIC+ACID-ADENYLATE+ESTER'>ANP</scene>, <scene name='pdbligand=BGC:BETA-D-GLUCOSE'>BGC</scene>, <scene name='pdbligand=K:POTASSIUM+ION'>K</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene></td></tr>
-	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Glucokinase Glucokinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.2 2.7.1.2] </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=3fgu FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3fgu OCA], [https://pdbe.org/3fgu PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3fgu RCSB], [https://www.ebi.ac.uk/pdbsum/3fgu PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3fgu ProSAT]</span></td></tr>
-	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://proteopedia.org/fgij/fg.htm?mol=3fgu FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3fgu OCA], [~~http~~://pdbe.org/3fgu PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3fgu RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3fgu PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3fgu ProSAT]</span></td></tr>	+
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/HXK4_HUMAN HXK4_HUMAN]] Defects in GCK are the cause of maturity-onset diabetes of the young type 2 (MODY2) [MIM:[~~http~~://omim.org/entry/125851 125851]]; also shortened MODY-2. MODY 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:1502186</ref> <ref>PMID:1464666</ref> <ref>PMID:1303265</ref> <ref>PMID:8495817</ref> <ref>PMID:8325892</ref> <ref>PMID:8446612</ref> <ref>PMID:8168652</ref> <ref>PMID:9049484</ref> <ref>PMID:10694920</ref> <ref>PMID:9662401</ref> <ref>PMID:10588527</ref> <ref>PMID:11106831</ref> <ref>PMID:11372010</ref> Defects in GCK are the cause of familial hyperinsulinemic hypoglycemia type 3 (HHF3) [MIM:[~~http~~://omim.org/entry/602485 602485]]; also known as persistent hyperinsulinemic hypoglycemia of infancy (PHHI) or congenital hyperinsulinism. HHF is the most common cause of persistent hypoglycemia in infancy. Unless early and aggressive intervention is undertaken, brain damage from recurrent episodes of hypoglycemia may occur.<ref>PMID:9435328</ref>	+	[https://www.uniprot.org/uniprot/HXK4_HUMAN HXK4_HUMAN] Defects in GCK are the cause of maturity-onset diabetes of the young type 2 (MODY2) [MIM:[https://omim.org/entry/125851 125851]; also shortened MODY-2. MODY 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:1502186</ref> <ref>PMID:1464666</ref> <ref>PMID:1303265</ref> <ref>PMID:8495817</ref> <ref>PMID:8325892</ref> <ref>PMID:8446612</ref> <ref>PMID:8168652</ref> <ref>PMID:9049484</ref> <ref>PMID:10694920</ref> <ref>PMID:9662401</ref> <ref>PMID:10588527</ref> <ref>PMID:11106831</ref> <ref>PMID:11372010</ref> Defects in GCK are the cause of familial hyperinsulinemic hypoglycemia type 3 (HHF3) [MIM:[https://omim.org/entry/602485 602485]; also known as persistent hyperinsulinemic hypoglycemia of infancy (PHHI) or congenital hyperinsulinism. HHF is the most common cause of persistent hypoglycemia in infancy. Unless early and aggressive intervention is undertaken, brain damage from recurrent episodes of hypoglycemia may occur.<ref>PMID:9435328</ref>
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/HXK4_HUMAN HXK4_HUMAN]] Catalyzes the initial step in utilization of glucose by the beta-cell and liver at physiological glucose concentration. Glucokinase has a high Km for glucose, and so it is effective only when glucose is abundant. The role of GCK is to provide G6P for the synthesis of glycogen. Pancreatic glucokinase plays an important role in modulating insulin secretion. Hepatic glucokinase helps to facilitate the uptake and conversion of glucose by acting as an insulin-sensitive determinant of hepatic glucose usage.	+	[https://www.uniprot.org/uniprot/HXK4_HUMAN HXK4_HUMAN] Catalyzes the initial step in utilization of glucose by the beta-cell and liver at physiological glucose concentration. Glucokinase has a high Km for glucose, and so it is effective only when glucose is abundant. The role of GCK is to provide G6P for the synthesis of glycogen. Pancreatic glucokinase plays an important role in modulating insulin secretion. Hepatic glucokinase helps to facilitate the uptake and conversion of glucose by acting as an insulin-sensitive determinant of hepatic glucose usage.
	== 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: ~~Glucokinase]]~~	+	[[Category: Homo sapiens]]
-	~~[[Category: Human~~]]	+
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Boutin~~, J A~~]]	+	[[Category: Boutin JA]]
-	[[Category: Ferry, G]]	+	[[Category: Ferry G]]
-	[[Category: Lagarde, A]]	+	[[Category: Lagarde A]]
-	[[Category: Petit, P]]	+	[[Category: Petit P]]
-	[[Category: Vuillard, L]]	+	[[Category: Vuillard L]]
-	~~[[Category: Atp-binding]]~~	+
-	~~[[Category: Diabetes mellitus]]~~	+
-	~~[[Category: Disease mutation]]~~	+
-	~~[[Category: Glycolysis]]~~	+
-	~~[[Category: Hexokinase iv]]~~	+
-	~~[[Category: Kinase]]~~	+
-	~~[[Category: Nucleotide-binding]]~~	+
-	~~[[Category: Transferase~~]]	+

OCA at 10:30, 9 September 2020

2020-09-09T10:30:22Z

←Older revision		Revision as of 10:30, 9 September 2020
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	==Catalytic complex of Human Glucokinase==		==Catalytic complex of Human Glucokinase==
-	<StructureSection load='3fgu' size='340' side='right' caption='[[3fgu]], [[Resolution\|resolution]] 2.15Å' scene=''>	+	<StructureSection load='3fgu' size='340' side='right'caption='[[3fgu]], [[Resolution\|resolution]] 2.15Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3fgu]] is a 1 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=3FGU OCA]. For a <b>guided tour on the structure components</b> use [http://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3FGU FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3fgu]] is a 1 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=3FGU OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=3FGU FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=ANP:PHOSPHOAMINOPHOSPHONIC+ACID-ADENYLATE+ESTER'>ANP</scene>, <scene name='pdbligand=BGC:BETA-D-GLUCOSE'>BGC</scene>, <scene name='pdbligand=K:POTASSIUM+ION'>K</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=ANP:PHOSPHOAMINOPHOSPHONIC+ACID-ADENYLATE+ESTER'>ANP</scene>, <scene name='pdbligand=BGC:BETA-D-GLUCOSE'>BGC</scene>, <scene name='pdbligand=K:POTASSIUM+ION'>K</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1v4s\|1v4s]], [[3f9m\|3f9m]], [[1v4t\|1v4t]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1v4s\|1v4s]], [[3f9m\|3f9m]], [[1v4t\|1v4t]]</td></tr>
	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Glucokinase Glucokinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.2 2.7.1.2] </span></td></tr>		<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Glucokinase Glucokinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.2 2.7.1.2] </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=3fgu FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3fgu OCA], [http://pdbe.org/3fgu PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3fgu RCSB], [http://www.ebi.ac.uk/pdbsum/3fgu PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3fgu ProSAT]</span></td></tr>	+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://proteopedia.org/fgij/fg.htm?mol=3fgu FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3fgu OCA], [http://pdbe.org/3fgu PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3fgu RCSB], [http://www.ebi.ac.uk/pdbsum/3fgu PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3fgu ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 34:		Line 34:

	==See Also==		==See Also==
-	*[[Hexokinase\|Hexokinase]]	+	*[[Hexokinase 3D structures\|Hexokinase 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
Line 41:		Line 41:
	[[Category: Glucokinase]]		[[Category: Glucokinase]]
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Boutin, J A]]		[[Category: Boutin, J A]]
	[[Category: Ferry, G]]		[[Category: Ferry, G]]

OCA at 08:10, 5 December 2018

2018-12-05T08:10:19Z

←Older revision		Revision as of 08:10, 5 December 2018
Line 1:		Line 1:
		+
	==Catalytic complex of Human Glucokinase==		==Catalytic complex of Human Glucokinase==
	<StructureSection load='3fgu' size='340' side='right' caption='[[3fgu]], [[Resolution\|resolution]] 2.15Å' scene=''>		<StructureSection load='3fgu' size='340' side='right' caption='[[3fgu]], [[Resolution\|resolution]] 2.15Å' scene=''>
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	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1v4s\|1v4s]], [[3f9m\|3f9m]], [[1v4t\|1v4t]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1v4s\|1v4s]], [[3f9m\|3f9m]], [[1v4t\|1v4t]]</td></tr>
	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Glucokinase Glucokinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.2 2.7.1.2] </span></td></tr>		<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Glucokinase Glucokinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.2 2.7.1.2] </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=3fgu FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3fgu OCA], [http://pdbe.org/3fgu PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3fgu RCSB], [http://www.ebi.ac.uk/pdbsum/3fgu 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=3fgu FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3fgu OCA], [http://pdbe.org/3fgu PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3fgu RCSB], [http://www.ebi.ac.uk/pdbsum/3fgu PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3fgu ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 16:		Line 17:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/fg/3fgu_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/fg/3fgu_consurf.spt"</scriptWhenChecked>
	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>		<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>

OCA at 05:55, 7 February 2016

2016-02-07T05:55:11Z

←Older revision		Revision as of 05:55, 7 February 2016
Line 2:		Line 2:
	<StructureSection load='3fgu' size='340' side='right' caption='[[3fgu]], [[Resolution\|resolution]] 2.15Å' scene=''>		<StructureSection load='3fgu' size='340' side='right' caption='[[3fgu]], [[Resolution\|resolution]] 2.15Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3fgu]] is a 1 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=3FGU OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3FGU FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3fgu]] is a 1 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=3FGU OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3FGU FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=ANP:PHOSPHOAMINOPHOSPHONIC+ACID-ADENYLATE+ESTER'>ANP</scene>, <scene name='pdbligand=BGC:BETA-D-GLUCOSE'>BGC</scene>, <scene name='pdbligand=K:POTASSIUM+ION'>K</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=ANP:PHOSPHOAMINOPHOSPHONIC+ACID-ADENYLATE+ESTER'>ANP</scene>, <scene name='pdbligand=BGC:BETA-D-GLUCOSE'>BGC</scene>, <scene name='pdbligand=K:POTASSIUM+ION'>K</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1v4s\|1v4s]], [[3f9m\|3f9m]], [[1v4t\|1v4t]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1v4s\|1v4s]], [[3f9m\|3f9m]], [[1v4t\|1v4t]]</td></tr>
	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Glucokinase Glucokinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.2 2.7.1.2] </span></td></tr>		<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Glucokinase Glucokinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.2 2.7.1.2] </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=3fgu FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3fgu OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3fgu RCSB], [http://www.ebi.ac.uk/pdbsum/3fgu 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=3fgu FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3fgu OCA], [http://pdbe.org/3fgu PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3fgu RCSB], [http://www.ebi.ac.uk/pdbsum/3fgu PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 20:		Line 20:
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>
	</jmolCheckbox>		</jmolCheckbox>
-	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/~~chain_selection~~.php?pdb_ID=~~2ata~~ ConSurf].	+	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=3fgu ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
Line 30:		Line 30:
	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>		From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
	</div>		</div>
		+	<div class="pdbe-citations 3fgu" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 38:		Line 39:
	</StructureSection>		</StructureSection>
	[[Category: Glucokinase]]		[[Category: Glucokinase]]
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Boutin, J A]]		[[Category: Boutin, J A]]
	[[Category: Ferry, G]]		[[Category: Ferry, G]]

OCA at 14:26, 18 December 2014

2014-12-18T14:26:53Z

←Older revision		Revision as of 14:26, 18 December 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_3fgu~~\| ~~PDB~~=3fgu \| ~~SCENE~~= }}	+	==Catalytic complex of Human Glucokinase==
-	===~~Catalytic complex~~ of ~~Human~~ Glucokinase===	+	<StructureSection load='3fgu' size='340' side='right' caption='[[3fgu]], [[Resolution\|resolution]] 2.15Å' scene=''>
-	~~{{ABSTRACT_PUBMED_22101819}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[3fgu]] is a 1 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=3FGU OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3FGU FirstGlance]. <br>
		+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=ANP:PHOSPHOAMINOPHOSPHONIC+ACID-ADENYLATE+ESTER'>ANP</scene>, <scene name='pdbligand=BGC:BETA-D-GLUCOSE'>BGC</scene>, <scene name='pdbligand=K:POTASSIUM+ION'>K</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene></td></tr>
		+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1v4s\|1v4s]], [[3f9m\|3f9m]], [[1v4t\|1v4t]]</td></tr>
		+	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Glucokinase Glucokinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.2 2.7.1.2] </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=3fgu FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3fgu OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3fgu RCSB], [http://www.ebi.ac.uk/pdbsum/3fgu PDBsum]</span></td></tr>
		+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/HXK4_HUMAN HXK4_HUMAN]] Defects in GCK are the cause of maturity-onset diabetes of the young type 2 (MODY2) [MIM:[http://omim.org/entry/125851 125851]]; also shortened MODY-2. MODY 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:1502186</ref> <ref>PMID:1464666</ref> <ref>PMID:1303265</ref> <ref>PMID:8495817</ref> <ref>PMID:8325892</ref> <ref>PMID:8446612</ref> <ref>PMID:8168652</ref> <ref>PMID:9049484</ref> <ref>PMID:10694920</ref> <ref>PMID:9662401</ref> <ref>PMID:10588527</ref> <ref>PMID:11106831</ref> <ref>PMID:11372010</ref> Defects in GCK are the cause of familial hyperinsulinemic hypoglycemia type 3 (HHF3) [MIM:[http://omim.org/entry/602485 602485]]; also known as persistent hyperinsulinemic hypoglycemia of infancy (PHHI) or congenital hyperinsulinism. HHF is the most common cause of persistent hypoglycemia in infancy. Unless early and aggressive intervention is undertaken, brain damage from recurrent episodes of hypoglycemia may occur.<ref>PMID:9435328</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/HXK4_HUMAN HXK4_HUMAN]] Catalyzes the initial step in utilization of glucose by the beta-cell and liver at physiological glucose concentration. Glucokinase has a high Km for glucose, and so it is effective only when glucose is abundant. The role of GCK is to provide G6P for the synthesis of glycogen. Pancreatic glucokinase plays an important role in modulating insulin secretion. Hepatic glucokinase helps to facilitate the uptake and conversion of glucose by acting as an insulin-sensitive determinant of hepatic glucose usage.
		+	== 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/fg/3fgu_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 ==
		+	Glucokinase (GK) catalyses the formation of glucose 6-phosphate from glucose and ATP. A specific feature of GK amongst hexokinases is that it can cycle between active and inactive conformations as a function of glucose concentration, resulting in a unique positive kinetic cooperativity with glucose, which turns GK into a unique key sensor of glucose metabolism, notably in the pancreas. GK is a target of antidiabetic drugs aimed at the activation of GK activity, leading to insulin secretion. Here, the first structures of a GK-glucose complex without activator, of GK-glucose-AMP-PNP and of GK-glucose-AMP-PNP with a bound activator are reported. All these structures are extremely similar, thus demonstrating that binding of GK activators does not result in conformational changes of the active protein but in stabilization of the active form of GK.

-	~~==Disease==~~	+	The active conformation of human glucokinase is not altered by allosteric activators.,Petit P, Antoine M, Ferry G, Boutin JA, Lagarde A, Gluais L, Vincentelli R, Vuillard L Acta Crystallogr D Biol Crystallogr. 2011 Nov;67(Pt 11):929-35. Epub 2011 Oct 19. PMID:22101819<ref>PMID:22101819</ref>
-	[[http://www.uniprot.org/uniprot/HXK4_HUMAN HXK4_HUMAN]] Defects in GCK are the cause of maturity-onset diabetes of the young type 2 (MODY2) [MIM:[http://omim.org/entry/125851 125851]]; also shortened MODY-2. MODY 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:1502186</ref><ref>PMID:1464666</ref><ref>PMID:1303265</ref><ref>PMID:8495817</ref><ref>PMID:8325892</ref><ref>PMID:8446612</ref><ref>PMID:8168652</ref><ref>PMID:9049484</ref><ref>PMID:10694920</ref><ref>PMID:9662401</ref><ref>PMID:10588527</ref><ref>PMID:11106831</ref><ref>PMID:11372010</ref> Defects in GCK are the cause of familial hyperinsulinemic hypoglycemia type 3 (~~HHF3~~) ~~[MIM~~:~~[http://omim~~.org/entry/602485 602485]]; also known as persistent hyperinsulinemic hypoglycemia of infancy (PHHI) or congenital hyperinsulinism. HHF is the most common cause of persistent hypoglycemia in infancy. Unless early and aggressive intervention is undertaken, brain damage from recurrent episodes of hypoglycemia may occur.<ref>PMID:~~9435328~~</ref>	+

-	~~==Function==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[http:~~/~~/www.uniprot.org/uniprot/HXK4_HUMAN HXK4_HUMAN]] Catalyzes the initial step in utilization of glucose by the beta-cell and liver at physiological glucose concentration. Glucokinase has~~ a ~~high Km for glucose, and so it is effective only when glucose is abundant. The role~~ of ~~GCK is to provide G6P for~~ the ~~synthesis of glycogen~~. ~~Pancreatic glucokinase plays an important role in modulating insulin secretion~~. ~~Hepatic glucokinase helps to facilitate the uptake and conversion of glucose by acting as an insulin-sensitive determinant~~ of ~~hepatic glucose usage~~.	+	</div>
-		+
-	~~==About this Structure==~~	+
-	~~[[3fgu]] is a 1 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=3FGU OCA].~~	+

	==See Also==		==See Also==
	*[[Hexokinase\|Hexokinase]]		*[[Hexokinase\|Hexokinase]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:022101819</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Glucokinase]]		[[Category: Glucokinase]]
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Boutin, J A.]]	+	[[Category: Boutin, J A]]
-	[[Category: Ferry, G.]]	+	[[Category: Ferry, G]]
-	[[Category: Lagarde, A.]]	+	[[Category: Lagarde, A]]
-	[[Category: Petit, P.]]	+	[[Category: Petit, P]]
-	[[Category: Vuillard, L.]]	+	[[Category: Vuillard, L]]
	[[Category: Atp-binding]]		[[Category: Atp-binding]]
	[[Category: Diabetes mellitus]]		[[Category: Diabetes mellitus]]
	[[Category: Disease mutation]]		[[Category: Disease mutation]]
-	[[Category: Glucokinase]]
	[[Category: Glycolysis]]		[[Category: Glycolysis]]
	[[Category: Hexokinase iv]]		[[Category: Hexokinase iv]]

OCA at 11:55, 24 March 2013

2013-03-24T11:55:05Z

←Older revision		Revision as of 11:55, 24 March 2013
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-	[[Image:3fgu.png\|left\|200px]]
-
	{{STRUCTURE_3fgu\| PDB=3fgu \| SCENE= }}		{{STRUCTURE_3fgu\| PDB=3fgu \| SCENE= }}
-
	===Catalytic complex of Human Glucokinase===		===Catalytic complex of Human Glucokinase===
		+	{{ABSTRACT_PUBMED_22101819}}

-	~~{{ABSTRACT_PUBMED_22101819}}~~	+	==Disease==
		+	[[http://www.uniprot.org/uniprot/HXK4_HUMAN HXK4_HUMAN]] Defects in GCK are the cause of maturity-onset diabetes of the young type 2 (MODY2) [MIM:[http://omim.org/entry/125851 125851]]; also shortened MODY-2. MODY 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:1502186</ref><ref>PMID:1464666</ref><ref>PMID:1303265</ref><ref>PMID:8495817</ref><ref>PMID:8325892</ref><ref>PMID:8446612</ref><ref>PMID:8168652</ref><ref>PMID:9049484</ref><ref>PMID:10694920</ref><ref>PMID:9662401</ref><ref>PMID:10588527</ref><ref>PMID:11106831</ref><ref>PMID:11372010</ref> Defects in GCK are the cause of familial hyperinsulinemic hypoglycemia type 3 (HHF3) [MIM:[http://omim.org/entry/602485 602485]]; also known as persistent hyperinsulinemic hypoglycemia of infancy (PHHI) or congenital hyperinsulinism. HHF is the most common cause of persistent hypoglycemia in infancy. Unless early and aggressive intervention is undertaken, brain damage from recurrent episodes of hypoglycemia may occur.<ref>PMID:9435328</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/HXK4_HUMAN HXK4_HUMAN]] Catalyzes the initial step in utilization of glucose by the beta-cell and liver at physiological glucose concentration. Glucokinase has a high Km for glucose, and so it is effective only when glucose is abundant. The role of GCK is to provide G6P for the synthesis of glycogen. Pancreatic glucokinase plays an important role in modulating insulin secretion. Hepatic glucokinase helps to facilitate the uptake and conversion of glucose by acting as an insulin-sensitive determinant of hepatic glucose usage.

	==About this Structure==		==About this Structure==
Line 14:		Line 16:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:022101819</ref><references group="xtra"/>	+	<ref group="xtra">PMID:022101819</ref><references group="xtra"/><references/>
	[[Category: Glucokinase]]		[[Category: Glucokinase]]
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]

OCA at 05:46, 20 October 2012

2012-10-20T05:46:40Z

←Older revision		Revision as of 05:46, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[3fgu]] is a 1 chain structure ~~of [[Hexokinase]]~~ 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=3FGU OCA].	+	[[3fgu]] is a 1 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=3FGU OCA].

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

OCA at 11:05, 25 July 2012

2012-07-25T11:05:22Z

←Older revision		Revision as of 11:05, 25 July 2012
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	[[Image:3fgu.png\|left\|200px]]		[[Image:3fgu.png\|left\|200px]]

-	<!--
-	The line below this paragraph, containing "STRUCTURE_3fgu", 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_3fgu\| PDB=3fgu \| SCENE= }}		{{STRUCTURE_3fgu\| PDB=3fgu \| SCENE= }}

	===Catalytic complex of Human Glucokinase===		===Catalytic complex of Human Glucokinase===

-
-	<!--
-	The line below this paragraph, {{ABSTRACT_PUBMED_22101819}}, adds the Publication Abstract to the page
-	(as it appears on PubMed at http://www.pubmed.gov), where 22101819 is the PubMed ID number.
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	{{ABSTRACT_PUBMED_22101819}}		{{ABSTRACT_PUBMED_22101819}}

OCA at 08:30, 25 April 2012

2012-04-25T08:30:37Z

←Older revision		Revision as of 08:30, 25 April 2012
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	===Catalytic complex of Human Glucokinase===		===Catalytic complex of Human Glucokinase===

		+
		+	<!--
		+	The line below this paragraph, {{ABSTRACT_PUBMED_22101819}}, adds the Publication Abstract to the page
		+	(as it appears on PubMed at http://www.pubmed.gov), where 22101819 is the PubMed ID number.
		+	-->
		+	{{ABSTRACT_PUBMED_22101819}}

	==About this Structure==		==About this Structure==
Line 16:		Line 22:

	==See Also==		==See Also==
-	*[[Hexokinase]]	+	*[[Hexokinase\|Hexokinase]]
		+
		+	==Reference==
		+	<ref group="xtra">PMID:022101819</ref><references group="xtra"/>
	[[Category: Glucokinase]]		[[Category: Glucokinase]]
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]

OCA: Protected "3fgu" [edit=sysop:move=sysop]

2011-11-09T11:00:45Z

Protected "3fgu" [edit=sysop:move=sysop]

←Older revision

Revision as of 11:00, 9 November 2011