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10.1159/000233241 http://scihub22266oqcxt.onion/10.1159/000233241 19710529!3711575!19710529     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Physiol+Biochem 2009 ; 24 (3-4): 153-60 Nephropedia Template TP {{tp|p=19710529|t=2009. Chloroquine blocks a mutant Kir2 1 channel responsible for short QT syndrome and normalizes repolarization properties in silico |pdf=|usr=}}{{19710529}} gab.com Text Chloroquine blocks a mutant Kir2 1 channel responsible for short QT syndrome and normalizes repolarization properties in silico JO: Cell Physiol Biochem http://www.kidney.de/pget.php?&tw=1&pmid=19710529 #FOAvip Short QT Syndrome (SQTS) is a novel clinical entity characterized by markedly rapid cardiac repolarization and lethal arrhythmias. A mutation in the Kir2.1 inward rectifier K+ channel (D172N) causes one form of SQTS (SQT3). Pharmacologic block of Kir2.1 channels may hold promise as potential therapy for SQT3. We recently reported that the anti-malarial drug chloroquine blocks Kir2.1 channels by plugging the cytoplasmic pore domain. In this study, we tested whether chloroquine blocks D172N Kir2.1 channels in a heterologous expression system and if chloroquine normalizes repolarization properties using a mathematical model of a human ventricular myocyte. Chloroquine caused a dose- and voltage-dependent reduction in wild-type (WT), D172N and WT-D172N heteromeric Kir2.1 current. The potency and kinetics of chloroquine block of D172N and WT-D172N Kir2.1 current were similar to WT. In silico modeling of the heterozygous WT-D172N Kir2.1 condition predicted that 3 microM chloroquine normalized inward rectifier K+ current magnitude, action potential duration and effective refractory period. Our results suggest that therapeutic concentrations of chloroquine might lengthen cardiac repolarization in SQT3. Twit Text FOAVip Chloroquine blocks a mutant Kir2 1 channel responsible for short QT syndrome and normalizes repolarization properties in silico ????Cell Physiol Biochem http://www.kidney.de/pget.php?&tw=1&pmid=19710529 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19710529 #FOAvip English Wikipedia <ref>{{Cite pmid|19710529}}</ref> Chloroquine blocks a mutant Kir2 1 channel responsible for short QT syndrome and normalizes repolarization properties in silico #MMPMID19710529 Lopez-Izquierdo A; Ponce-Balbuena D; Ferrer T; Sachse FB; Tristani-Firouzi M; Sanchez-Chapula JA Cell Physiol Biochem 2009[]; 24 (3-4): 153-60 PMID19710529show ga Short QT Syndrome (SQTS) is a novel clinical entity characterized by markedly rapid cardiac repolarization and lethal arrhythmias. A mutation in the Kir2.1 inward rectifier K+ channel (D172N) causes one form of SQTS (SQT3). Pharmacologic block of Kir2.1 channels may hold promise as potential therapy for SQT3. We recently reported that the anti-malarial drug chloroquine blocks Kir2.1 channels by plugging the cytoplasmic pore domain. In this study, we tested whether chloroquine blocks D172N Kir2.1 channels in a heterologous expression system and if chloroquine normalizes repolarization properties using a mathematical model of a human ventricular myocyte. Chloroquine caused a dose- and voltage-dependent reduction in wild-type (WT), D172N and WT-D172N heteromeric Kir2.1 current. The potency and kinetics of chloroquine block of D172N and WT-D172N Kir2.1 current were similar to WT. In silico modeling of the heterozygous WT-D172N Kir2.1 condition predicted that 3 microM chloroquine normalized inward rectifier K+ current magnitude, action potential duration and effective refractory period. Our results suggest that therapeutic concentrations of chloroquine might lengthen cardiac repolarization in SQT3. |Action Potentials/drug effects/genetics[MESH] |Antimalarials/*pharmacology[MESH] |Cell Line[MESH] |Chloroquine/*pharmacology[MESH] |Computer Simulation[MESH] |Dose-Response Relationship, Drug[MESH] |Electrophysiology[MESH] |Heart Ventricles/cytology[MESH] |Humans[MESH] |Kidney/cytology[MESH] |Membrane Potentials/drug effects/genetics/physiology[MESH] |Models, Statistical[MESH] |Mutation/drug effects[MESH] |Myocytes, Cardiac/drug effects[MESH] |Patch-Clamp Techniques[MESH] |Potassium Channel Blockers/*pharmacology[MESH] |Potassium Channels, Inwardly Rectifying/*genetics/physiology[MESH]Chloroquine blocks a mutant Kir2 1 channel responsible for short QT sy(epmc).pdf DeepDyve Pubget Overpricing