Inhibition of AP-1 signaling by JDP2 overexpression protects cardiomyocytes against hypertrophy and apoptosis induction

Cardiovascular Research

Volumn 99, Issue 1, 2013, Pages 121-128

  Hill, Christian ^a   Würfel, Alona ^a   Heger, Jacqueline ^a   Meyering, Bettina ^a   Schlüter, Klaus Dieter ^a   Weber, Martin ^a   Ferdinandy, Peter ^b   Aronheim, Ami ^c   Schulz, Rainer ^a   Euler, Gerhild ^a  

^a JUSTUS LIEBIG UNIVERSITY   (Germany)

^b SEMMELWEIS UNIVERSITY   (Hungary)

^c TECHNION ISRAEL INSTITUTE OF TECHNOLOGY   (Israel)

Author keywords

Apoptosis; Cardiac; Contractile function; Hypertrophy; Remodeling; Transcription factor AP 1

Indexed keywords

CALCIUM; ISOPRENALINE; JDP2 PROTEIN; PROTEIN C JUN; TRANSCRIPTION FACTOR AP 1; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CALCIUM CELL LEVEL; CELL ISOLATION; CELL SIZE; CELL STIMULATION; CONTROLLED STUDY; CROSS-SECTIONAL STUDY; ELECTROSTIMULATION; HEART HYPERTROPHY; HEART MUSCLE CELL; HEART MUSCLE CONTRACTILITY; HEART MUSCLE RELAXATION; HEART PROTECTION; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN SYNTHESIS;

APOPTOSIS; CARDIAC; CONTRACTILE FUNCTION; HYPERTROPHY; REMODELING; TRANSCRIPTION FACTOR AP-1;

ADRENERGIC BETA-AGONISTS; ANIMALS; APOPTOSIS; CARDIOMEGALY; CELLS, CULTURED; DOSE-RESPONSE RELATIONSHIP, DRUG; ELECTRIC STIMULATION; MICE; MICE, INBRED C57BL; MICE, TRANSGENIC; MYOCARDIAL CONTRACTION; MYOCYTES, CARDIAC; REPRESSOR PROTEINS; SIGNAL TRANSDUCTION; TIME FACTORS; TRANSCRIPTION FACTOR AP-1; TRANSFORMING GROWTH FACTOR BETA1; UP-REGULATION; VENTRICULAR REMODELING;

EID: 84879366398     PISSN: 00086363     EISSN: 17553245     Source Type: Journal    
DOI: 10.1093/cvr/cvt094     Document Type: Article

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