Loss of K+ currents in heart failure is accentuated in KChIP2 deficient mice

Journal of Cardiovascular Electrophysiology

Volumn 25, Issue 8, 2014, Pages 896-904

  Grubb, SØren ^a   Speerschneider, Tobias ^a   Occhipinti, Dona ^a   Fiset, Céline ^c   Olesen, SØren Peter ^a   Thomsen, Morten B ^a   Calloe, Kirstine ^a,b  

^a UNIVERSITY OF COPENHAGEN   (Denmark)

^b UNIVERSITY OF COPENHAGEN   (Denmark)

^c MONTREAL HEART INSTITUTE   (Canada)

Author keywords

action potentials; cardiac; heart failure; KChIP2; potassium currents; repolarization; transient outward potassium current

Indexed keywords

KCNIP2 PROTEIN, MOUSE; KV CHANNEL INTERACTING PROTEIN; POTASSIUM;

ACTION POTENTIAL; ANIMAL; C57BL MOUSE; DEFICIENCY; DISEASE MODEL; DOWN REGULATION; GENETICS; GENOTYPE; HEART FAILURE; HEART MUSCLE CELL; HEART MUSCLE CONDUCTION SYSTEM; HEART PACING; KNOCKOUT MOUSE; MALE; METABOLISM; PATHOPHYSIOLOGY; PHENOTYPE; TIME;

ACTION POTENTIALS; ANIMALS; CARDIAC PACING, ARTIFICIAL; DISEASE MODELS, ANIMAL; DOWN-REGULATION; GENOTYPE; HEART CONDUCTION SYSTEM; HEART FAILURE; KV CHANNEL-INTERACTING PROTEINS; MALE; MICE, INBRED C57BL; MICE, KNOCKOUT; MYOCYTES, CARDIAC; PHENOTYPE; POTASSIUM; TIME FACTORS;

EID: 84905870255     PISSN: 10453873     EISSN: 15408167     Source Type: Journal    
DOI: 10.1111/jce.12422     Document Type: Article

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