Pharmacological modification of gap junction coupling by an antiarrhythmic peptide via protein kinase C activation.

The FASEB journal : official publication of the Federation of American Societies for Experimental Biology

Volumn 16, Issue 9, 2002, Pages 1114-1116

  Weng, Stephan ^a   Lauven, Melani ^a   Schaefer, Thomas ^a   Polontchouk, Lioudmila ^a   Grover, Rajiv ^a   Dhein, Stefan ^a  

^a UNIVERSITY OF LEIPZIG   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

AAP 10; ANTIARRHYTHMIC AGENT; CONNEXIN 43; ISOENZYME; MEMBRANE PROTEIN; OLIGOPEPTIDE; PEPTIDE; PRKCA PROTEIN, HUMAN; PROTEIN KINASE C; PROTEIN KINASE C ALPHA;

ANIMAL; ARTICLE; BIOLOGICAL MODEL; CELL CULTURE; CELL JUNCTION; DRUG EFFECT; ELECTRIC CONDUCTIVITY; ENZYME ACTIVATION; ENZYMOLOGY; GUINEA PIG; HEART; HEART MUSCLE; HELA CELL; HUMAN; ION TRANSPORT; METABOLISM; PHYSIOLOGY;

ANIMALS; ANTI-ARRHYTHMIA AGENTS; CELLS, CULTURED; CONNEXIN 43; ELECTRIC CONDUCTIVITY; ENZYME ACTIVATION; GAP JUNCTIONS; GUINEA PIGS; HEART; HELA CELLS; HUMANS; ION TRANSPORT; ISOENZYMES; MEMBRANE PROTEINS; MODELS, BIOLOGICAL; MYOCARDIUM; OLIGOPEPTIDES; PEPTIDES; PROTEIN KINASE C; PROTEIN KINASE C-ALPHA;

MLCS; MLOWN;

EID: 0036634865     PISSN: None     EISSN: 15306860     Source Type: Journal    
DOI: 10.1096/fj.01-0918fje     Document Type: Article

References (0)