2le7 - Revision history

OCA at 05:42, 15 May 2024

2024-05-15T05:42:09Z

←Older revision		Revision as of 05:42, 15 May 2024
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	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2le7]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2LE7 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2LE7 FirstGlance]. <br>		<table><tr><td colspan='2'>[[2le7]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2LE7 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2LE7 FirstGlance]. <br>
-	</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=2le7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2le7 OCA], [https://pdbe.org/2le7 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2le7 RCSB], [https://www.ebi.ac.uk/pdbsum/2le7 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2le7 ProSAT]</span></td></tr>	+	</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">Solution NMR</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=2le7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2le7 OCA], [https://pdbe.org/2le7 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2le7 RCSB], [https://www.ebi.ac.uk/pdbsum/2le7 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2le7 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==

OCA at 08:57, 14 June 2023

2023-06-14T08:57:08Z

←Older revision		Revision as of 08:57, 14 June 2023
Line 1:		Line 1:

	==Solution nmr structure of the S4S5 linker of herg potassium channel==		==Solution nmr structure of the S4S5 linker of herg potassium channel==
-	<StructureSection load='2le7' size='340' side='right'caption='[[2le7~~]], [[NMR_Ensembles_of_Models \| 20 NMR models~~]]' scene=''>	+	<StructureSection load='2le7' size='340' side='right'caption='[[2le7]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2le7]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2LE7 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2LE7 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2le7]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2LE7 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2LE7 FirstGlance]. <br>
	</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=2le7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2le7 OCA], [https://pdbe.org/2le7 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2le7 RCSB], [https://www.ebi.ac.uk/pdbsum/2le7 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2le7 ProSAT]</span></td></tr>		</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=2le7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2le7 OCA], [https://pdbe.org/2le7 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2le7 RCSB], [https://www.ebi.ac.uk/pdbsum/2le7 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2le7 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/KCNH2_HUMAN KCNH2_HUMAN]] Defects in KCNH2 are the cause of long QT syndrome type 2 (LQT2) [MIM:[https://omim.org/entry/613688 613688]]. Long QT syndromes are heart disorders characterized by a prolonged QT interval on the ECG and polymorphic ventricular arrhythmias. They cause syncope and sudden death in response to exercise or emotional stress. Deafness is often associated with LQT2.<ref>PMID:16361248</ref> <ref>PMID:9600240</ref> <ref>PMID:7889573</ref> <ref>PMID:8914737</ref> <ref>PMID:8635257</ref> <ref>PMID:8877771</ref> <ref>PMID:9024139</ref> <ref>PMID:9693036</ref> <ref>PMID:9544837</ref> <ref>PMID:9452080</ref> <ref>PMID:10086971</ref> <ref>PMID:10220144</ref> <ref>PMID:10187793</ref> <ref>PMID:10517660</ref> <ref>PMID:10735633</ref> <ref>PMID:10973849</ref> <ref>PMID:10862094</ref> <ref>PMID:10753933</ref> <ref>PMID:12062363</ref> <ref>PMID:12354768</ref> <ref>PMID:12621127</ref> <ref>PMID:15051636</ref> <ref>PMID:15840476</ref> <ref>PMID:22314138</ref> Defects in KCNH2 are the cause of short QT syndrome type 1 (SQT1) [MIM:[https://omim.org/entry/609620 609620]]. Short QT syndromes are heart disorders characterized by idiopathic persistently and uniformly short QT interval on ECG in the absence of structural heart disease in affected individuals. They cause syncope and sudden death.<ref>PMID:14676148</ref> <ref>PMID:15828882</ref>	+	[https://www.uniprot.org/uniprot/KCNH2_HUMAN KCNH2_HUMAN] Defects in KCNH2 are the cause of long QT syndrome type 2 (LQT2) [MIM:[https://omim.org/entry/613688 613688]. Long QT syndromes are heart disorders characterized by a prolonged QT interval on the ECG and polymorphic ventricular arrhythmias. They cause syncope and sudden death in response to exercise or emotional stress. Deafness is often associated with LQT2.<ref>PMID:16361248</ref> <ref>PMID:9600240</ref> <ref>PMID:7889573</ref> <ref>PMID:8914737</ref> <ref>PMID:8635257</ref> <ref>PMID:8877771</ref> <ref>PMID:9024139</ref> <ref>PMID:9693036</ref> <ref>PMID:9544837</ref> <ref>PMID:9452080</ref> <ref>PMID:10086971</ref> <ref>PMID:10220144</ref> <ref>PMID:10187793</ref> <ref>PMID:10517660</ref> <ref>PMID:10735633</ref> <ref>PMID:10973849</ref> <ref>PMID:10862094</ref> <ref>PMID:10753933</ref> <ref>PMID:12062363</ref> <ref>PMID:12354768</ref> <ref>PMID:12621127</ref> <ref>PMID:15051636</ref> <ref>PMID:15840476</ref> <ref>PMID:22314138</ref> Defects in KCNH2 are the cause of short QT syndrome type 1 (SQT1) [MIM:[https://omim.org/entry/609620 609620]. Short QT syndromes are heart disorders characterized by idiopathic persistently and uniformly short QT interval on ECG in the absence of structural heart disease in affected individuals. They cause syncope and sudden death.<ref>PMID:14676148</ref> <ref>PMID:15828882</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/KCNH2_HUMAN KCNH2_HUMAN]] Pore-forming (alpha) subunit of voltage-gated inwardly rectifying potassium channel. Channel properties are modulated by cAMP and subunit assembly. Mediates the rapidly activating component of the delayed rectifying potassium current in heart (IKr). Isoform 3 has no channel activity by itself, but modulates channel characteristics when associated with isoform 1.	+	[https://www.uniprot.org/uniprot/KCNH2_HUMAN KCNH2_HUMAN] Pore-forming (alpha) subunit of voltage-gated inwardly rectifying potassium channel. Channel properties are modulated by cAMP and subunit assembly. Mediates the rapidly activating component of the delayed rectifying potassium current in heart (IKr). Isoform 3 has no channel activity by itself, but modulates channel characteristics when associated with isoform 1.
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 23:		Line 23:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Kuchel~~, P W~~]]	+	[[Category: Kuchel PW]]
-	[[Category: Ng~~, C A~~]]	+	[[Category: Ng CA]]
-	[[Category: Vandenberg~~, J I]]~~	+	[[Category: Vandenberg JI]]
-	~~[[Category: Herg]]~~	+
-	~~[[Category: Membrane protein]]~~	+
-	~~[[Category: S4s5]]~~	+
-	~~[[Category: Transport protein]]~~	+
-	~~[[Category: Voltage-gated potassium channel~~]]	+

OCA at 07:51, 9 February 2022

2022-02-09T07:51:07Z

←Older revision		Revision as of 07:51, 9 February 2022
Line 3:		Line 3:
	<StructureSection load='2le7' size='340' side='right'caption='[[2le7]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>		<StructureSection load='2le7' size='340' side='right'caption='[[2le7]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2le7]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2LE7 OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://proteopedia.org/fgij/fg.htm?mol=2LE7 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2le7]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2LE7 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2LE7 FirstGlance]. <br>
-	</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=2le7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2le7 OCA], [~~http~~://pdbe.org/2le7 PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=2le7 RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/2le7 PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=2le7 ProSAT]</span></td></tr>	+	</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=2le7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2le7 OCA], [https://pdbe.org/2le7 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2le7 RCSB], [https://www.ebi.ac.uk/pdbsum/2le7 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2le7 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/KCNH2_HUMAN KCNH2_HUMAN]] Defects in KCNH2 are the cause of long QT syndrome type 2 (LQT2) [MIM:[~~http~~://omim.org/entry/613688 613688]]. Long QT syndromes are heart disorders characterized by a prolonged QT interval on the ECG and polymorphic ventricular arrhythmias. They cause syncope and sudden death in response to exercise or emotional stress. Deafness is often associated with LQT2.<ref>PMID:16361248</ref> <ref>PMID:9600240</ref> <ref>PMID:7889573</ref> <ref>PMID:8914737</ref> <ref>PMID:8635257</ref> <ref>PMID:8877771</ref> <ref>PMID:9024139</ref> <ref>PMID:9693036</ref> <ref>PMID:9544837</ref> <ref>PMID:9452080</ref> <ref>PMID:10086971</ref> <ref>PMID:10220144</ref> <ref>PMID:10187793</ref> <ref>PMID:10517660</ref> <ref>PMID:10735633</ref> <ref>PMID:10973849</ref> <ref>PMID:10862094</ref> <ref>PMID:10753933</ref> <ref>PMID:12062363</ref> <ref>PMID:12354768</ref> <ref>PMID:12621127</ref> <ref>PMID:15051636</ref> <ref>PMID:15840476</ref> <ref>PMID:22314138</ref> Defects in KCNH2 are the cause of short QT syndrome type 1 (SQT1) [MIM:[~~http~~://omim.org/entry/609620 609620]]. Short QT syndromes are heart disorders characterized by idiopathic persistently and uniformly short QT interval on ECG in the absence of structural heart disease in affected individuals. They cause syncope and sudden death.<ref>PMID:14676148</ref> <ref>PMID:15828882</ref>	+	[[https://www.uniprot.org/uniprot/KCNH2_HUMAN KCNH2_HUMAN]] Defects in KCNH2 are the cause of long QT syndrome type 2 (LQT2) [MIM:[https://omim.org/entry/613688 613688]]. Long QT syndromes are heart disorders characterized by a prolonged QT interval on the ECG and polymorphic ventricular arrhythmias. They cause syncope and sudden death in response to exercise or emotional stress. Deafness is often associated with LQT2.<ref>PMID:16361248</ref> <ref>PMID:9600240</ref> <ref>PMID:7889573</ref> <ref>PMID:8914737</ref> <ref>PMID:8635257</ref> <ref>PMID:8877771</ref> <ref>PMID:9024139</ref> <ref>PMID:9693036</ref> <ref>PMID:9544837</ref> <ref>PMID:9452080</ref> <ref>PMID:10086971</ref> <ref>PMID:10220144</ref> <ref>PMID:10187793</ref> <ref>PMID:10517660</ref> <ref>PMID:10735633</ref> <ref>PMID:10973849</ref> <ref>PMID:10862094</ref> <ref>PMID:10753933</ref> <ref>PMID:12062363</ref> <ref>PMID:12354768</ref> <ref>PMID:12621127</ref> <ref>PMID:15051636</ref> <ref>PMID:15840476</ref> <ref>PMID:22314138</ref> Defects in KCNH2 are the cause of short QT syndrome type 1 (SQT1) [MIM:[https://omim.org/entry/609620 609620]]. Short QT syndromes are heart disorders characterized by idiopathic persistently and uniformly short QT interval on ECG in the absence of structural heart disease in affected individuals. They cause syncope and sudden death.<ref>PMID:14676148</ref> <ref>PMID:15828882</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/KCNH2_HUMAN KCNH2_HUMAN]] Pore-forming (alpha) subunit of voltage-gated inwardly rectifying potassium channel. Channel properties are modulated by cAMP and subunit assembly. Mediates the rapidly activating component of the delayed rectifying potassium current in heart (IKr). Isoform 3 has no channel activity by itself, but modulates channel characteristics when associated with isoform 1.	+	[[https://www.uniprot.org/uniprot/KCNH2_HUMAN KCNH2_HUMAN]] Pore-forming (alpha) subunit of voltage-gated inwardly rectifying potassium channel. Channel properties are modulated by cAMP and subunit assembly. Mediates the rapidly activating component of the delayed rectifying potassium current in heart (IKr). Isoform 3 has no channel activity by itself, but modulates channel characteristics when associated with isoform 1.
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==

OCA at 07:03, 6 May 2020

2020-05-06T07:03:11Z

←Older revision		Revision as of 07:03, 6 May 2020
Line 1:		Line 1:

	==Solution nmr structure of the S4S5 linker of herg potassium channel==		==Solution nmr structure of the S4S5 linker of herg potassium channel==
-	<StructureSection load='2le7' size='340' side='right' caption='[[2le7]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>	+	<StructureSection load='2le7' size='340' side='right'caption='[[2le7]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[2le7]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2LE7 OCA]. For a <b>guided tour on the structure components</b> use [http://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=2LE7 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[2le7]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2LE7 OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=2LE7 FirstGlance]. <br>
-	</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=2le7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2le7 OCA], [http://pdbe.org/2le7 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2le7 RCSB], [http://www.ebi.ac.uk/pdbsum/2le7 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2le7 ProSAT]</span></td></tr>	+	</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=2le7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2le7 OCA], [http://pdbe.org/2le7 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2le7 RCSB], [http://www.ebi.ac.uk/pdbsum/2le7 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2le7 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 23:		Line 23:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Large Structures]]
	[[Category: Kuchel, P W]]		[[Category: Kuchel, P W]]
	[[Category: Ng, C A]]		[[Category: Ng, C A]]

OCA at 19:47, 1 August 2018

2018-08-01T19:47:48Z

←Older revision		Revision as of 19:47, 1 August 2018
Line 1:		Line 1:
		+
	==Solution nmr structure of the S4S5 linker of herg potassium channel==		==Solution nmr structure of the S4S5 linker of herg potassium channel==
	<StructureSection load='2le7' size='340' side='right' caption='[[2le7]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>		<StructureSection load='2le7' size='340' side='right' caption='[[2le7]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2le7]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2LE7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2LE7 FirstGlance]. <br>		<table><tr><td colspan='2'>[[2le7]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2LE7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2LE7 FirstGlance]. <br>
-	</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=2le7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2le7 OCA], [http://pdbe.org/2le7 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2le7 RCSB], [http://www.ebi.ac.uk/pdbsum/2le7 PDBsum]</span></td></tr>	+	</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=2le7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2le7 OCA], [http://pdbe.org/2le7 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2le7 RCSB], [http://www.ebi.ac.uk/pdbsum/2le7 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=2le7 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==

OCA at 13:52, 11 September 2015

2015-09-11T13:52:57Z

←Older revision		Revision as of 13:52, 11 September 2015
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[2le7]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2LE7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2LE7 FirstGlance]. <br>		<table><tr><td colspan='2'>[[2le7]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2LE7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2LE7 FirstGlance]. <br>
-	</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=2le7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2le7 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2le7 RCSB], [http://www.ebi.ac.uk/pdbsum/2le7 PDBsum]</span></td></tr>	+	</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=2le7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2le7 OCA], [http://pdbe.org/2le7 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=2le7 RCSB], [http://www.ebi.ac.uk/pdbsum/2le7 PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 17:		Line 17:
	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 2le7" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>

OCA at 12:22, 18 December 2014

2014-12-18T12:22:11Z

←Older revision		Revision as of 12:22, 18 December 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_2le7\| PDB=2le7 \| SCENE= }}~~	+	==Solution nmr structure of the S4S5 linker of herg potassium channel==
-	===Solution nmr structure of the S4S5 linker of herg potassium channel===	+	<StructureSection load='2le7' size='340' side='right' caption='[[2le7]], [[NMR_Ensembles_of_Models \| 20 NMR models]]' scene=''>
-	~~{{ABSTRACT_PUBMED_22359612}}~~	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[2le7]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2LE7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2LE7 FirstGlance]. <br>
-	==Disease==	+	</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=2le7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2le7 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2le7 RCSB], [http://www.ebi.ac.uk/pdbsum/2le7 PDBsum]</span></td></tr>
-	[[http://www.uniprot.org/uniprot/KCNH2_HUMAN KCNH2_HUMAN]] Defects in KCNH2 are the cause of long QT syndrome type 2 (LQT2) [MIM:[http://omim.org/entry/613688 613688]]. Long QT syndromes are heart disorders characterized by a prolonged QT interval on the ECG and polymorphic ventricular arrhythmias. They cause syncope and sudden death in response to exercise or emotional stress. Deafness is often associated with LQT2.<ref>PMID:16361248</ref><ref>PMID:9600240</ref><ref>PMID:7889573</ref><ref>PMID:8914737</ref><ref>PMID:8635257</ref><ref>PMID:8877771</ref><ref>PMID:9024139</ref><ref>PMID:9693036</ref><ref>PMID:9544837</ref><ref>PMID:9452080</ref><ref>PMID:10086971</ref><ref>PMID:10220144</ref><ref>PMID:10187793</ref><ref>PMID:10517660</ref><ref>PMID:10735633</ref><ref>PMID:10973849</ref><ref>PMID:10862094</ref><ref>PMID:10753933</ref><ref>PMID:12062363</ref><ref>PMID:12354768</ref><ref>PMID:12621127</ref><ref>PMID:15051636</ref><ref>PMID:15840476</ref><ref>PMID:22314138</ref> Defects in KCNH2 are the cause of short QT syndrome type 1 (SQT1) [MIM:[http://omim.org/entry/609620 609620]]. Short QT syndromes are heart disorders characterized by idiopathic persistently and uniformly short QT interval on ECG in the absence of structural heart disease in affected individuals. They cause syncope and sudden death.<ref>PMID:14676148</ref><ref>PMID:15828882</ref>	+	</table>
-		+	== Disease ==
-	==Function==	+	[[http://www.uniprot.org/uniprot/KCNH2_HUMAN KCNH2_HUMAN]] Defects in KCNH2 are the cause of long QT syndrome type 2 (LQT2) [MIM:[http://omim.org/entry/613688 613688]]. Long QT syndromes are heart disorders characterized by a prolonged QT interval on the ECG and polymorphic ventricular arrhythmias. They cause syncope and sudden death in response to exercise or emotional stress. Deafness is often associated with LQT2.<ref>PMID:16361248</ref> <ref>PMID:9600240</ref> <ref>PMID:7889573</ref> <ref>PMID:8914737</ref> <ref>PMID:8635257</ref> <ref>PMID:8877771</ref> <ref>PMID:9024139</ref> <ref>PMID:9693036</ref> <ref>PMID:9544837</ref> <ref>PMID:9452080</ref> <ref>PMID:10086971</ref> <ref>PMID:10220144</ref> <ref>PMID:10187793</ref> <ref>PMID:10517660</ref> <ref>PMID:10735633</ref> <ref>PMID:10973849</ref> <ref>PMID:10862094</ref> <ref>PMID:10753933</ref> <ref>PMID:12062363</ref> <ref>PMID:12354768</ref> <ref>PMID:12621127</ref> <ref>PMID:15051636</ref> <ref>PMID:15840476</ref> <ref>PMID:22314138</ref> Defects in KCNH2 are the cause of short QT syndrome type 1 (SQT1) [MIM:[http://omim.org/entry/609620 609620]]. Short QT syndromes are heart disorders characterized by idiopathic persistently and uniformly short QT interval on ECG in the absence of structural heart disease in affected individuals. They cause syncope and sudden death.<ref>PMID:14676148</ref> <ref>PMID:15828882</ref>
		+	== Function ==
	[[http://www.uniprot.org/uniprot/KCNH2_HUMAN KCNH2_HUMAN]] Pore-forming (alpha) subunit of voltage-gated inwardly rectifying potassium channel. Channel properties are modulated by cAMP and subunit assembly. Mediates the rapidly activating component of the delayed rectifying potassium current in heart (IKr). Isoform 3 has no channel activity by itself, but modulates channel characteristics when associated with isoform 1.		[[http://www.uniprot.org/uniprot/KCNH2_HUMAN KCNH2_HUMAN]] Pore-forming (alpha) subunit of voltage-gated inwardly rectifying potassium channel. Channel properties are modulated by cAMP and subunit assembly. Mediates the rapidly activating component of the delayed rectifying potassium current in heart (IKr). Isoform 3 has no channel activity by itself, but modulates channel characteristics when associated with isoform 1.
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Human ether-a-go-go-related gene (hERG) K(+) channels have unusual gating kinetics. Characterised by slow activation/deactivation but rapid inactivation/recovery from inactivation, the unique gating kinetics underlie the central role hERG channels play in cardiac repolarisation. The slow activation and deactivation kinetics are regulated in part by the S4-S5 linker, which couples movement of the voltage sensor domain to opening of the activation gate at the distal end of the inner helix of the pore domain. It has also been suggested that cytosolic domains may interact with the S4-S5 linker to regulate activation and deactivation kinetics. Here, we show that the solution structure of a peptide corresponding to the S4-S5 linker of hERG contains an amphipathic helix. The effects of mutations at the majority of residues in the S4-S5 linker of hERG were consistent with the previously identified role in coupling voltage sensor movement to the activation gate. However, mutations to Ser543, Tyr545, Gly546 and Ala548 had more complex phenotypes indicating that these residues are involved in additional interactions. We propose a model in which the S4-S5 linker, in addition to coupling VSD movement to the activation gate, also contributes to interactions that stabilise the closed state and a separate set of interactions that stabilise the open state. The S4-S5 linker therefore acts as a signal integrator and plays a crucial role in the slow deactivation kinetics of the channel.

-	~~==About this Structure==~~	+	The S4-S5 linker acts as a signal integrator for HERG K+ channel activation and deactivation gating.,Ng CA, Perry MD, Tan PS, Hill AP, Kuchel PW, Vandenberg JI PLoS One. 2012;7(2):e31640. Epub 2012 Feb 16. PMID:22359612<ref>PMID:22359612</ref>
-	~~[[2le7]] is~~ a ~~1 chain structure~~. ~~Full experimental information is available from [http~~:~~//oca~~.~~weizmann~~.~~ac.il~~/~~oca-bin/ocashort?id=2LE7 OCA].~~	+

-	==~~Reference~~==	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~<ref group="xtra">PMID:022359612</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	</div>
-	[[Category: Kuchel, P W.]]	+	== References ==
-	[[Category: Ng, C A.]]	+	<references/>
-	[[Category: Vandenberg, J I.]]	+	__TOC__
		+	</StructureSection>
		+	[[Category: Kuchel, P W]]
		+	[[Category: Ng, C A]]
		+	[[Category: Vandenberg, J I]]
	[[Category: Herg]]		[[Category: Herg]]
	[[Category: Membrane protein]]		[[Category: Membrane protein]]

OCA at 18:45, 24 March 2013

2013-03-24T18:45:33Z

←Older revision		Revision as of 18:45, 24 March 2013
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-	[[Image:2le7.jpg\|left\|200px]]
-
-	<!--
-	The line below this paragraph, containing "STRUCTURE_2le7", 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_2le7\| PDB=2le7 \| SCENE= }}		{{STRUCTURE_2le7\| PDB=2le7 \| SCENE= }}
-
	===Solution nmr structure of the S4S5 linker of herg potassium channel===		===Solution nmr structure of the S4S5 linker of herg potassium channel===
		+	{{ABSTRACT_PUBMED_22359612}}

		+	==Disease==
		+	[[http://www.uniprot.org/uniprot/KCNH2_HUMAN KCNH2_HUMAN]] Defects in KCNH2 are the cause of long QT syndrome type 2 (LQT2) [MIM:[http://omim.org/entry/613688 613688]]. Long QT syndromes are heart disorders characterized by a prolonged QT interval on the ECG and polymorphic ventricular arrhythmias. They cause syncope and sudden death in response to exercise or emotional stress. Deafness is often associated with LQT2.<ref>PMID:16361248</ref><ref>PMID:9600240</ref><ref>PMID:7889573</ref><ref>PMID:8914737</ref><ref>PMID:8635257</ref><ref>PMID:8877771</ref><ref>PMID:9024139</ref><ref>PMID:9693036</ref><ref>PMID:9544837</ref><ref>PMID:9452080</ref><ref>PMID:10086971</ref><ref>PMID:10220144</ref><ref>PMID:10187793</ref><ref>PMID:10517660</ref><ref>PMID:10735633</ref><ref>PMID:10973849</ref><ref>PMID:10862094</ref><ref>PMID:10753933</ref><ref>PMID:12062363</ref><ref>PMID:12354768</ref><ref>PMID:12621127</ref><ref>PMID:15051636</ref><ref>PMID:15840476</ref><ref>PMID:22314138</ref> Defects in KCNH2 are the cause of short QT syndrome type 1 (SQT1) [MIM:[http://omim.org/entry/609620 609620]]. Short QT syndromes are heart disorders characterized by idiopathic persistently and uniformly short QT interval on ECG in the absence of structural heart disease in affected individuals. They cause syncope and sudden death.<ref>PMID:14676148</ref><ref>PMID:15828882</ref>

-	~~<!--~~	+	==Function==
-	~~The line below this paragraph, {{ABSTRACT_PUBMED_22359612}}, adds the Publication Abstract to the page~~	+	[[http://www.uniprot.org/uniprot/KCNH2_HUMAN KCNH2_HUMAN]] Pore-forming (alpha) subunit of voltage-gated inwardly rectifying potassium channel. Channel properties are modulated by cAMP and subunit assembly. Mediates the rapidly activating component of the delayed rectifying potassium current in heart (IKr). Isoform 3 has no channel activity by itself, but modulates channel characteristics when associated with isoform 1.
-	~~(as it appears on PubMed at~~ http://www.~~pubmed~~.~~gov~~)~~, where 22359612 is~~ the ~~PubMed ID number~~.	+
-	~~-->~~	+
-	~~{{ABSTRACT_PUBMED_22359612}}~~	+

	==About this Structure==		==About this Structure==
Line 22:		Line 13:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:022359612</ref><references group="xtra"/>	+	<ref group="xtra">PMID:022359612</ref><references group="xtra"/><references/>
	[[Category: Kuchel, P W.]]		[[Category: Kuchel, P W.]]
	[[Category: Ng, C A.]]		[[Category: Ng, C A.]]

OCA at 09:11, 25 April 2012

2012-04-25T09:11:22Z

←Older revision		Revision as of 09:11, 25 April 2012
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-	~~'''Unreleased structure'''~~	+	[[Image:2le7.jpg\|left\|200px]]

-	The ~~entry 2le7~~ is ~~ON HOLD~~ ~~until Paper Publication~~	+	<!--
		+	The line below this paragraph, containing "STRUCTURE_2le7", 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_2le7\| PDB=2le7 \| SCENE= }}

-	~~Authors: Ng, C.A., Kuchel, P.W., Vandenberg, J.I.~~	+	===Solution nmr structure of the S4S5 linker of herg potassium channel===

-	~~Description~~: ~~Solution nmr structure of~~ the ~~S4S5 linker of herg~~ potassium channel	+
		+	<!--
		+	The line below this paragraph, {{ABSTRACT_PUBMED_22359612}}, adds the Publication Abstract to the page
		+	(as it appears on PubMed at http://www.pubmed.gov), where 22359612 is the PubMed ID number.
		+	-->
		+	{{ABSTRACT_PUBMED_22359612}}
		+
		+	==About this Structure==
		+	[[2le7]] is a 1 chain structure. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2LE7 OCA].
		+
		+	==Reference==
		+	<ref group="xtra">PMID:022359612</ref><references group="xtra"/>
		+	[[Category: Kuchel, P W.]]
		+	[[Category: Ng, C A.]]
		+	[[Category: Vandenberg, J I.]]
		+	[[Category: Herg]]
		+	[[Category: Membrane protein]]
		+	[[Category: S4s5]]
		+	[[Category: Transport protein]]
		+	[[Category: Voltage-gated potassium channel]]

OCA at 05:28, 29 June 2011

2011-06-29T05:28:04Z

←Older revision		Revision as of 05:28, 29 June 2011
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 2le7 is ON HOLD	+	The entry 2le7 is ON HOLD until Paper Publication

	Authors: Ng, C.A., Kuchel, P.W., Vandenberg, J.I.		Authors: Ng, C.A., Kuchel, P.W., Vandenberg, J.I.

-	Description: ~~SOLUTION NMR STRUCTURE OF THE~~ S4S5 ~~LINKER OF HERG POTASSIUM CHANNEL~~	+	Description: Solution nmr structure of the S4S5 linker of herg potassium channel