3qic - Revision history

OCA at 17:13, 1 November 2023

OCA — Wed, 01 Nov 2023 17:13:14 GMT

←Older revision		Revision as of 17:13, 1 November 2023
Line 3:		Line 3:
	<StructureSection load='3qic' size='340' side='right'caption='[[3qic]], [[Resolution\|resolution]] 2.20Å' scene=''>		<StructureSection load='3qic' size='340' side='right'caption='[[3qic]], [[Resolution\|resolution]] 2.20Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3qic]] is a 1 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=3QIC OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3QIC FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3qic]] 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=3QIC OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3QIC FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=GLC:ALPHA~~-~~D-GLUCOSE'>GLC</scene>~~, ~~<scene name='pdbligand=GOL:GLYCEROL'>GOL</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]] 2.2Å</td></tr>
-	<tr id='~~NonStdRes~~'><td class="sblockLbl"><b>[[~~Non-Standard_Residue~~\|~~NonStd Res~~:]]</b></td><td class="sblockDat"><scene name='pdbligand=~~SEP~~:~~PHOSPHOSERINE~~'>~~SEP~~</scene><~~/td></tr>~~	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GLC:ALPHA-D-GLUCOSE'>GLC</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</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;'>[[1v4s\|1v4s]]~~, ~~[[3id8\|3id8]], [[3f9m\|3f9m]]~~<~~/div></td></tr>~~	+
-	~~<tr id~~='~~gene'><td class~~=~~"sblockLbl"><b>[[Gene\|Gene~~:~~]]</b></td><td class="sblockDat">GCK ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>~~	+
-	~~<tr id='activity~~'>~~<td class="sblockLbl"><b>Activity:~~</b></td><td class="sblockDat"><span class='plainlinks'>[https://en.wikipedia.org/wiki/Glucokinase Glucokinase], with EC number [https://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=3qic FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qic OCA], [https://pdbe.org/3qic PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3qic RCSB], [https://www.ebi.ac.uk/pdbsum/3qic PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3qic 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=3qic FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qic OCA], [https://pdbe.org/3qic PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3qic RCSB], [https://www.ebi.ac.uk/pdbsum/3qic PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3qic ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[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>	+	[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 ==
-	[[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.	+	[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.
	<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: ~~Glucokinase]]~~	+	[[Category: Homo sapiens]]
-	~~[[Category: Human~~]]	+
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Liu, J]]	+	[[Category: Liu J]]
-	[[Category: Liu, Q]]	+	[[Category: Liu Q]]
-	[[Category: Liu, S]]	+	[[Category: Liu S]]
-	~~[[Category: Glycolysis]]~~	+
-	~~[[Category: Kinase]]~~	+
-	~~[[Category: Phosphorylation]]~~	+
-	~~[[Category: Sugar binding]]~~	+
-	~~[[Category: Transferase~~]]	+

OCA at 06:10, 8 June 2022

OCA — Wed, 08 Jun 2022 06:10:05 GMT

←Older revision		Revision as of 06:10, 8 June 2022
Line 1:		Line 1:

	==The structure of human glucokinase E339K mutation==		==The structure of human glucokinase E339K mutation==
-	<StructureSection load='3qic' size='340' side='right' caption='[[3qic]], [[Resolution\|resolution]] 2.20Å' scene=''>	+	<StructureSection load='3qic' size='340' side='right'caption='[[3qic]], [[Resolution\|resolution]] 2.20Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3qic]] 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=3QIC OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3QIC FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3qic]] is a 1 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=3QIC OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3QIC FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GLC:ALPHA-D-GLUCOSE'>GLC</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GLC:ALPHA-D-GLUCOSE'>GLC</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene></td></tr>
-	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1v4s\|1v4s]], [[3id8\|3id8]], [[3f9m\|3f9m]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[1v4s\|1v4s]], [[3id8\|3id8]], [[3f9m\|3f9m]]</div></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">GCK ([~~http~~://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">GCK ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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'>[https://en.wikipedia.org/wiki/Glucokinase Glucokinase], with EC number [https://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=3qic FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qic OCA], [~~http~~://pdbe.org/3qic PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3qic RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3qic PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3qic 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=3qic FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qic OCA], [https://pdbe.org/3qic PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3qic RCSB], [https://www.ebi.ac.uk/pdbsum/3qic PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3qic 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.
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 24:		Line 24:
	</div>		</div>
	<div class="pdbe-citations 3qic" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 3qic" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[Hexokinase 3D structures\|Hexokinase 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
Line 30:		Line 33:
	[[Category: Glucokinase]]		[[Category: Glucokinase]]
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Liu, J]]		[[Category: Liu, J]]
	[[Category: Liu, Q]]		[[Category: Liu, Q]]

OCA at 09:15, 8 November 2017

OCA — Wed, 08 Nov 2017 09:15:22 GMT

←Older revision		Revision as of 09:15, 8 November 2017
Line 24:		Line 24:
	</div>		</div>
	<div class="pdbe-citations 3qic" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 3qic" style="background-color:#fffaf0;"></div>
-
-	==See Also==
-	*[[Hexokinase\|Hexokinase]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 11:33, 5 August 2016

OCA — Fri, 05 Aug 2016 11:33:47 GMT

←Older revision		Revision as of 11:33, 5 August 2016
Line 1:		Line 1:
		+
	==The structure of human glucokinase E339K mutation==		==The structure of human glucokinase E339K mutation==
	<StructureSection load='3qic' size='340' side='right' caption='[[3qic]], [[Resolution\|resolution]] 2.20Å' scene=''>		<StructureSection load='3qic' size='340' side='right' caption='[[3qic]], [[Resolution\|resolution]] 2.20Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3qic]] 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=3QIC OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3QIC FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3qic]] 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=3QIC OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3QIC FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GLC:ALPHA-D-GLUCOSE'>GLC</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GLC:ALPHA-D-GLUCOSE'>GLC</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1v4s\|1v4s]], [[3id8\|3id8]], [[3f9m\|3f9m]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1v4s\|1v4s]], [[3id8\|3id8]], [[3f9m\|3f9m]]</td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">GCK ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">GCK ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=3qic FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qic OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3qic RCSB], [http://www.ebi.ac.uk/pdbsum/3qic 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=3qic FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qic OCA], [http://pdbe.org/3qic PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3qic RCSB], [http://www.ebi.ac.uk/pdbsum/3qic PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3qic ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 22:		Line 23:
	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 3qic" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 30:		Line 32:
	</StructureSection>		</StructureSection>
	[[Category: Glucokinase]]		[[Category: Glucokinase]]
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Liu, J]]		[[Category: Liu, J]]
	[[Category: Liu, Q]]		[[Category: Liu, Q]]

OCA at 11:03, 19 December 2014

OCA — Fri, 19 Dec 2014 11:03:02 GMT

←Older revision		Revision as of 11:03, 19 December 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_3qic~~\| ~~PDB~~=3qic \| ~~SCENE~~= }}	+	==The structure of human glucokinase E339K mutation==
-	===The ~~structure~~ of ~~human~~ glucokinase ~~E339K mutation~~===	+	<StructureSection load='3qic' size='340' side='right' caption='[[3qic]], [[Resolution\|resolution]] 2.20Å' scene=''>
-	~~{{ABSTRACT_PUBMED_21420961}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[3qic]] 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=3QIC OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3QIC FirstGlance]. <br>
		+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GLC:ALPHA-D-GLUCOSE'>GLC</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene></td></tr>
		+	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene></td></tr>
		+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1v4s\|1v4s]], [[3id8\|3id8]], [[3f9m\|3f9m]]</td></tr>
		+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">GCK ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</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=3qic FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qic OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3qic RCSB], [http://www.ebi.ac.uk/pdbsum/3qic 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.
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Human glucokinase (GK) plays an important role in glucose homeostasis. An E339K mutation in GK was recently found to be associated with hyperglycemia. It showed lower enzyme activity and impaired protein stability compared to the wild-type enzyme. Here, we present the crystal structure of E339K GK in complex with glucose. This mutation results in a conformational change of His416, spatially interfering with adenosine-triphosphate (ATP) binding. Furthermore, Ser411 at the ATP binding site is phosphorylated and then hydrogen bonded with Thr82, physically blocking the ATP binding. These findings provide structural basis for the reduced activity of this mutant.

-	~~==Disease==~~	+	Crystal structure of E339K mutated human glucokinase reveals changes in the ATP binding site.,Liu Q, Shen Y, Liu S, Weng J, Liu J FEBS Lett. 2011 Apr 20;585(8):1175-9. Epub 2011 Mar 22. PMID:21420961<ref>PMID:21420961</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==~~	+
-	~~[[3qic]] 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=3QIC OCA].~~	+

	==See Also==		==See Also==
	*[[Hexokinase\|Hexokinase]]		*[[Hexokinase\|Hexokinase]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:021420961</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Glucokinase]]		[[Category: Glucokinase]]
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Liu, J.]]	+	[[Category: Liu, J]]
-	[[Category: Liu, Q.]]	+	[[Category: Liu, Q]]
-	[[Category: Liu, S.]]	+	[[Category: Liu, S]]
	[[Category: Glycolysis]]		[[Category: Glycolysis]]
	[[Category: Kinase]]		[[Category: Kinase]]

OCA at 21:24, 24 March 2013

OCA — Sun, 24 Mar 2013 21:24:53 GMT

←Older revision		Revision as of 21:24, 24 March 2013
Line 1:		Line 1:
-	[[Image:3qic.png\|left\|200px]]
-
	{{STRUCTURE_3qic\| PDB=3qic \| SCENE= }}		{{STRUCTURE_3qic\| PDB=3qic \| SCENE= }}
-
	===The structure of human glucokinase E339K mutation===		===The structure of human glucokinase E339K mutation===
		+	{{ABSTRACT_PUBMED_21420961}}

-	~~{{ABSTRACT_PUBMED_21420961}}~~	+	==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:021420961</ref><references group="xtra"/>	+	<ref group="xtra">PMID:021420961</ref><references group="xtra"/><references/>
	[[Category: Glucokinase]]		[[Category: Glucokinase]]
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]

OCA at 20:00, 20 October 2012

OCA — Sat, 20 Oct 2012 20:00:05 GMT

←Older revision		Revision as of 20:00, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[3qic]] 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=3QIC OCA].	+	[[3qic]] 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=3QIC OCA].

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

OCA at 09:07, 27 July 2012

OCA — Fri, 27 Jul 2012 09:07:16 GMT

←Older revision		Revision as of 09:07, 27 July 2012
Line 1:		Line 1:
-	[[Image:3qic.~~jpg~~\|left\|200px]]	+	[[Image:3qic.png\|left\|200px]]

-	<!--
-	The line below this paragraph, containing "STRUCTURE_3qic", 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_3qic\| PDB=3qic \| SCENE= }}		{{STRUCTURE_3qic\| PDB=3qic \| SCENE= }}

	===The structure of human glucokinase E339K mutation===		===The structure of human glucokinase E339K mutation===

-
-	<!--
-	The line below this paragraph, {{ABSTRACT_PUBMED_21420961}}, adds the Publication Abstract to the page
-	(as it appears on PubMed at http://www.pubmed.gov), where 21420961 is the PubMed ID number.
-	-->
	{{ABSTRACT_PUBMED_21420961}}		{{ABSTRACT_PUBMED_21420961}}

	==About this Structure==		==About this Structure==
-	[[3qic]] 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=3QIC OCA].	+	[[3qic]] 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=3QIC OCA].
		+
		+	==See Also==
		+	*[[Hexokinase\|Hexokinase]]

	==Reference==		==Reference==
Line 28:		Line 20:
	[[Category: Liu, Q.]]		[[Category: Liu, Q.]]
	[[Category: Liu, S.]]		[[Category: Liu, S.]]
		+	[[Category: Glycolysis]]
		+	[[Category: Kinase]]
		+	[[Category: Phosphorylation]]
		+	[[Category: Sugar binding]]
		+	[[Category: Transferase]]

OCA at 05:43, 1 June 2011

OCA — Wed, 01 Jun 2011 05:43:56 GMT

←Older revision		Revision as of 05:43, 1 June 2011
Line 1:		Line 1:
-	~~'''Unreleased structure'''~~	+	[[Image:3qic.jpg\|left\|200px]]

-	The ~~entry 3qic~~ is ~~ON HOLD~~ ~~until Paper Publication~~	+	<!--
		+	The line below this paragraph, containing "STRUCTURE_3qic", 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_3qic\| PDB=3qic \| SCENE= }}

-	~~Authors: Liu, Q., Liu, S., Liu, J.~~	+	===The structure of human glucokinase E339K mutation===

-	~~Description:~~ The structure ~~of human glucokinase E339K mutation~~	+
		+	<!--
		+	The line below this paragraph, {{ABSTRACT_PUBMED_21420961}}, adds the Publication Abstract to the page
		+	(as it appears on PubMed at http://www.pubmed.gov), where 21420961 is the PubMed ID number.
		+	-->
		+	{{ABSTRACT_PUBMED_21420961}}
		+
		+	==About this Structure==
		+	[[3qic]] 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=3QIC OCA].
		+
		+	==Reference==
		+	<ref group="xtra">PMID:021420961</ref><references group="xtra"/>
		+	[[Category: Glucokinase]]
		+	[[Category: Homo sapiens]]
		+	[[Category: Liu, J.]]
		+	[[Category: Liu, Q.]]
		+	[[Category: Liu, S.]]

OCA at 06:39, 2 March 2011

OCA — Wed, 02 Mar 2011 06:39:25 GMT

←Older revision		Revision as of 06:39, 2 March 2011
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 3qic is ON HOLD	+	The entry 3qic is ON HOLD until Paper Publication

	Authors: Liu, Q., Liu, S., Liu, J.		Authors: Liu, Q., Liu, S., Liu, J.

	Description: The structure of human glucokinase E339K mutation		Description: The structure of human glucokinase E339K mutation