Cardiac-specific PID1 overexpression enhances pressure overload-induced cardiac hypertrophy in mice

Cellular Physiology and Biochemistry

Volumn 35, Issue 5, 2015, Pages 1975-1985

  Liu, Yaoqiu ^a   Shen, Yahui ^a   Zhu, Jingai ^a   Liu, Ming ^a   Li, Xing ^a   Chen, Yumei ^a   Kong, Xiangqing ^a   Song, Guixian ^a   Qian, Lingmei ^a  

^a NANJING MEDICAL UNIVERSITY   (China)

Author keywords

Akt; Cardiac hypertrophy; MAPK; PID1

Indexed keywords

COLLAGEN TYPE 1; COLLAGEN TYPE 3; CONNECTIVE TISSUE GROWTH FACTOR; FIBRONECTIN; GLYCOGEN SYNTHASE KINASE 3BETA; MITOGEN ACTIVATED PROTEIN KINASE KINASE 1; MITOGEN ACTIVATED PROTEIN KINASE KINASE 2; MITOGEN ACTIVATED PROTEIN KINASE P38; PHOSPHOTYROSINE INTERACTION DOMAIN CONTAINING 1; PROTEIN; PROTEIN KINASE B; STRESS ACTIVATED PROTEIN KINASE 1; SYNAPTOPHYSIN; UNCLASSIFIED DRUG; CARRIER PROTEIN; MITOGEN ACTIVATED PROTEIN KINASE; MYOSIN HEAVY CHAIN; PID1 PROTEIN, HUMAN;

ANIMAL EXPERIMENT; ANIMAL MODEL; AORTA CONSTRICTION; ARTICLE; CONGESTIVE CARDIOMYOPATHY; CONTROLLED STUDY; DISEASE EXACERBATION; ECHOCARDIOGRAPHY; EMBRYO; ENZYME PHOSPHORYLATION; GENE EXPRESSION; HEART FAILURE; HEART LEFT VENTRICLE OVERLOAD; HEART MUSCLE FIBROSIS; HEART TRANSPLANTATION; HEART VENTRICLE HYPERTROPHY; HUMAN; HUMAN TISSUE; MALE; MOUSE; NONHUMAN; PRIORITY JOURNAL; REAL TIME POLYMERASE CHAIN REACTION; TRANSVERSE AORTIC CONSTRICTION; UPREGULATION; WESTERN BLOTTING; ANIMAL; ANTAGONISTS AND INHIBITORS; C57BL MOUSE; CARDIOMEGALY; DISEASE MODEL; ECHOGRAPHY; GENETICS; HEART MUSCLE; HEART VENTRICLE; METABOLISM; PATHOLOGY; PRESSURE; PROMOTER REGION; SIGNAL TRANSDUCTION; TRANSGENIC MOUSE;

MUS; MUS MUSCULUS;

ANIMALS; CARDIOMEGALY; CARRIER PROTEINS; DISEASE MODELS, ANIMAL; HEART FAILURE; HEART VENTRICLES; HUMANS; MALE; MICE; MICE, INBRED C57BL; MICE, TRANSGENIC; MITOGEN-ACTIVATED PROTEIN KINASES; MYOCARDIUM; MYOSIN HEAVY CHAINS; PRESSURE; PROMOTER REGIONS, GENETIC; PROTO-ONCOGENE PROTEINS C-AKT; REAL-TIME POLYMERASE CHAIN REACTION; SIGNAL TRANSDUCTION; UP-REGULATION;

EID: 84927915634     PISSN: 10158987     EISSN: 14219778     Source Type: Journal    
DOI: 10.1159/000374005     Document Type: Article

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