Genetic depletion of cardiac myocyte STAT-3 abolishes classical preconditioning

Cardiovascular Research

Volumn 63, Issue 4, 2004, Pages 611-616

  Smith, Robert M ^a   Suleman, Naushaad ^a   Lacerda, Lydia ^a   Opie, Lionel H ^a   Akira, Shizuo ^b   Chien, Kenneth R ^c   Sack, Michael N ^d  

^a UNIVERSITY OF CAPE TOWN   (South Africa)

^b OSAKA UNIVERSITY   (Japan)

^c UNIVERSITY OF CALIFORNIA   (United States)

^d NATIONAL HEART LUNG AND BLOOD INSTITUTE   (United States)

Author keywords

Ischemia; Preconditioning; Signal transduction

Indexed keywords

ADENOSINE; DIAZOXIDE; STAT3 PROTEIN; TUMOR NECROSIS FACTOR ALPHA;

ANIMAL CELL; ANIMAL MODEL; ARTICLE; BIOTECHNOLOGY; CELL ISOLATION; CELL VIABILITY; CONDITIONED REFLEX; CONTROLLED STUDY; DISEASE SIMULATION; EVALUATION; EXPOSURE; HEART INFARCTION SIZE; HEART MUSCLE CELL; HEART MUSCLE ISCHEMIA; HEART MUSCLE REPERFUSION; ISOLATED HEART; MALE; MODULATION; MOLECULE; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN DEFICIENCY; PROTEIN DEPLETION; PROTEIN FUNCTION; WILD TYPE;

ANIMALS; DNA-BINDING PROTEINS; ISCHEMIC PRECONDITIONING, MYOCARDIAL; MICE; MICE, KNOCKOUT; MYOCARDIAL ISCHEMIA; MYOCYTES, CARDIAC; PERFUSION; STAT3 TRANSCRIPTION FACTOR; TRANS-ACTIVATORS;

EID: 4043082106     PISSN: 00086363     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.cardiores.2004.06.019     Document Type: Article

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