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10.1016/j.yjmcc.2009.02.027 http://scihub22266oqcxt.onion/10.1016/j.yjmcc.2009.02.027 19285083!2765655!19285083     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=19285083&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       J+Mol+Cell+Cardiol 2009 ; 47 (5): 743-7 Nephropedia Template TP {{tp|p=19285083|t=2009. Action potential clamp and chloroquine sensitivity of mutant Kir2 1 channels responsible for variant 3 short QT syndrome |pdf=|usr=}}{{19285083}} gab.com Text Action potential clamp and chloroquine sensitivity of mutant Kir2 1 channels responsible for variant 3 short QT syndrome JO: J Mol Cell Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=19285083 #FOAvip Recently identified genetic forms of short QT syndrome (SQTS) are associated with an increased risk of arrhythmia and sudden death. The SQT3 variant is associated with an amino-acid substitution (D172N) in the KCNJ2-encoded Kir2.1 K+ channel. In this study, whole-cell action potential (AP) clamp recording from transiently transfected Chinese Hamster Ovary cells at 37 degrees C showed marked augmentation of outward Kir2.1 current through D172N channels, associated with right-ward voltage-shifts of peak repolarizing current during both ventricular and atrial AP commands. Peak outward current elicited by ventricular AP commands was inhibited by chloroquine with an IC50 of 2.45 microM for wild-type (WT) Kir2.1, of 3.30 microM for D172N-Kir2.1 alone and of 3.11 microM for co-expressed WT and D172N (P>0.05 for all). These findings establish chloroquine as an effective inhibitor of SQT3 mutant Kir2.1 channels. Twit Text FOAVip Action potential clamp and chloroquine sensitivity of mutant Kir2 1 channels responsible for variant 3 short QT syndrome ????J Mol Cell Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=19285083 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19285083 #FOAvip English Wikipedia <ref>{{Cite pmid|19285083}}</ref> Action potential clamp and chloroquine sensitivity of mutant Kir2 1 channels responsible for variant 3 short QT syndrome #MMPMID19285083 El Harchi A; McPate MJ; Zhang Yh; Zhang H; Hancox JC J Mol Cell Cardiol 2009[Nov]; 47 (5): 743-7 PMID19285083show ga Recently identified genetic forms of short QT syndrome (SQTS) are associated with an increased risk of arrhythmia and sudden death. The SQT3 variant is associated with an amino-acid substitution (D172N) in the KCNJ2-encoded Kir2.1 K+ channel. In this study, whole-cell action potential (AP) clamp recording from transiently transfected Chinese Hamster Ovary cells at 37 degrees C showed marked augmentation of outward Kir2.1 current through D172N channels, associated with right-ward voltage-shifts of peak repolarizing current during both ventricular and atrial AP commands. Peak outward current elicited by ventricular AP commands was inhibited by chloroquine with an IC50 of 2.45 microM for wild-type (WT) Kir2.1, of 3.30 microM for D172N-Kir2.1 alone and of 3.11 microM for co-expressed WT and D172N (P>0.05 for all). These findings establish chloroquine as an effective inhibitor of SQT3 mutant Kir2.1 channels. |Action Potentials/*drug effects/genetics[MESH] |Animals[MESH] |Antirheumatic Agents/*pharmacology[MESH] |Arrhythmias, Cardiac/*genetics/*metabolism[MESH] |CHO Cells[MESH] |Chloroquine/*pharmacology[MESH] |Cricetinae[MESH] |Cricetulus[MESH] |Electrophysiology[MESH] |Humans[MESH] |Patch-Clamp Techniques/*methods[MESH]Action potential clamp and chloroquine sensitivity of mutant Kir2 1 ch(epmc).pdf DeepDyve Pubget Overpricing