Overexpression of TNNI3K, a cardiac-specific MAPKKK, promotes cardiac dysfunction

Journal of Molecular and Cellular Cardiology

Volumn 54, Issue 1, 2013, Pages 101-111

  Tang, Hao ^a   Xiao, Kunhong ^a   Mao, Lan ^a   Rockman, Howard A ^a   Marchuk, Douglas A ^a  

^a DUKE UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

Cardiac remodeling; Kinase; TNNI3K

Indexed keywords

CARDIAC TROPONIN I INTERACTING KINASE; CONNECTIN; HEART ENZYME; ISOPROTEIN; SERINE; THREONINE; TYROSINE; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CARDIOMYOPATHY; CONTROLLED STUDY; DISEASE COURSE; ENZYME ACTIVITY; ENZYME ASSAY; ENZYME PHOSPHORYLATION; HEART LEFT VENTRICLE OVERLOAD; HEART VENTRICLE REMODELING; IN VITRO STUDY; IN VIVO STUDY; INTRACELLULAR SIGNALING; MALE; MECHANICAL STRESS; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN FUNCTION; PROTEIN LOCALIZATION; PROTEIN MODIFICATION; PROTEOMICS; SARCOMERE LENGTH; WILD TYPE;

AMINO ACID SEQUENCE; ANIMALS; FEMALE; GENE EXPRESSION; HEK293 CELLS; HUMANS; MALE; MAP KINASE KINASE KINASES; MICE; MICE, INBRED DBA; MICE, TRANSGENIC; MOLECULAR SEQUENCE DATA; MUSCLE PROTEINS; MYOCARDIUM; MYOCYTES, CARDIAC; ORGAN SIZE; ORGANELLE SIZE; PEPTIDE FRAGMENTS; PHOSPHORYLATION; PROTEIN ISOFORMS; PROTEIN KINASES; PROTEIN PROCESSING, POST-TRANSLATIONAL; SARCOMERES; SIGNAL TRANSDUCTION; STRESS, PHYSIOLOGICAL; VENTRICULAR DYSFUNCTION, LEFT; VENTRICULAR REMODELING;

MUS MUSCULUS;

EID: 84871716646     PISSN: 00222828     EISSN: 10958584     Source Type: Journal    
DOI: 10.1016/j.yjmcc.2012.10.004     Document Type: Article

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