mTOR inactivation in myocardium from infant mice rapidly leads to dilated cardiomyopathy due to translation defects and p53/JNK-mediated apoptosis

Journal of Molecular and Cellular Cardiology

Volumn 97, Issue , 2016, Pages 213-225

  Mazelin, Laetitia ^a,b   Panthu, Baptiste ^c   Nicot, Anne Sophie ^b   Belotti, Edwige ^a,b   Tintignac, Lionel ^d,e   Teixeira, Geoffrey ^a   Zhang, Qing ^b   Risson, Valérie ^a,b   Baas, Dominique ^a,b   Delaune, Emilie ^b   Derumeaux, Geneviève ^a   Taillandier, Daniel ^f   Ohlmann, Théophile ^c   Ovize, Michel ^a   Gangloff, Yann Gaël ^a,b   Schaeffer, Laurent ^a,b,g  

^a UNIVERSITÉ LYON 1   (France)

^b UNIVERSITÉ DE LYON   (France)

^c CENTRE INTERNATIONAL DE RECHERCHE EN INFECTIOLOGIE   (France)

^d UNIVERSITY HOSPITAL BASEL   (Switzerland)

^e University of Montpellier   (France)

^f CRNH AUVERGNE   (France)

^g EDOUARD HERRIOT HOSPITAL   (France)

Author keywords

Cardiomyocyte apoptosis; Heart postnatal development; MTOR; Myocardial metabolism; Signal transduction; Translation

Indexed keywords

ANKRD1 PROTEIN; CASPASE 3; CELL PROTEIN; HIPPO PROTEIN; HYPOXIA INDUCIBLE FACTOR 1ALPHA; MAMMALIAN TARGET OF RAPAMYCIN; MAMMALIAN TARGET OF RAPAMYCIN COMPLEX 1; MAMMALIAN TARGET OF RAPAMYCIN COMPLEX 2; MST1 PROTEIN; MYOGLOBIN; PIFITHRIN ALPHA; PROTEIN P53; PROTEIN P63; STRESS ACTIVATED PROTEIN KINASE; UNCLASSIFIED DRUG; ANKRD1 PROTEIN, MOUSE; BIOLOGICAL MARKER; MUSCLE PROTEIN; NUCLEAR PROTEIN; REPRESSOR PROTEIN; TARGET OF RAPAMYCIN KINASE;

ADULT; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CARDIAC MUSCLE; CARDIAC MUSCLE CELL; CELL DEATH; CELL GROWTH; CELL HYPOXIA; CELL VIABILITY; CONGESTIVE CARDIOMYOPATHY; CONTROLLED STUDY; DOWN REGULATION; ENZYME ACTIVATION; ENZYME INACTIVATION; HEART MUSCLE FIBROSIS; HEART VENTRICLE HYPERTROPHY; INFANT; KNOCKOUT MOUSE; MOLECULAR MECHANICS; MOUSE; NONHUMAN; OXYGEN SUPPLY; PERINATAL PERIOD; PRIORITY JOURNAL; PROTEIN DEFECT; PROTEIN DEFICIENCY; PROTEIN DEGRADATION; PROTEIN SYNTHESIS; UPREGULATION; ANIMAL; BIOPSY; CARDIOPULMONARY BYPASS; DISEASE MODEL; ECHOCARDIOGRAPHY; ENERGY METABOLISM; GENE EXPRESSION PROFILING; GENE EXPRESSION REGULATION; GENETICS; HEART FUNCTION TEST; METABOLISM; PATHOLOGY; PATHOPHYSIOLOGY; SIGNAL TRANSDUCTION;

ANIMALS; APOPTOSIS; BIOMARKERS; BIOPSY; CARDIOMYOPATHY, DILATED; CARDIOPULMONARY BYPASS; DISEASE MODELS, ANIMAL; ECHOCARDIOGRAPHY; ENERGY METABOLISM; GENE EXPRESSION PROFILING; GENE EXPRESSION REGULATION; HEART FUNCTION TESTS; JNK MITOGEN-ACTIVATED PROTEIN KINASES; MICE; MICE, KNOCKOUT; MUSCLE PROTEINS; MYOGLOBIN; NUCLEAR PROTEINS; PROTEIN BIOSYNTHESIS; PROTEOLYSIS; REPRESSOR PROTEINS; SIGNAL TRANSDUCTION; TOR SERINE-THREONINE KINASES; TUMOR SUPPRESSOR PROTEIN P53;

EID: 84974738112     PISSN: 00222828     EISSN: 10958584     Source Type: Journal    
DOI: 10.1016/j.yjmcc.2016.04.011     Document Type: Article

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