Depletion of extracellular signal-regulated kinase 1 in mice with cardiomyopathy caused by lamin A/C gene mutation partially prevents pathology before isoenzyme activation

Human Molecular Genetics

Volumn 23, Issue 1, 2014, Pages 1-11

  Wu, Wei ^a   Iwata, Shinichi ^a,b   Homma, Shunichi ^a   Worman, Howard J ^a   Muchir, Antoine ^a,c  

^a Columbia University ^*  (United States)

^b OSAKA CITY UNIVERSITY GRADUATE SCHOOL OF MEDICINE   (Japan)

^c INSERM   (France)

Author keywords

[No Author keywords available]

Indexed keywords

LAMIN A; LAMIN C; MITOGEN ACTIVATED PROTEIN KINASE 1; MITOGEN ACTIVATED PROTEIN KINASE 3;

ANIMAL TISSUE; ARTICLE; CARDIOMYOPATHY; ENZYME ACTIVATION; ENZYME ACTIVITY; GENE DELETION; GENOTYPE; HEART FUNCTION; HEART LEFT VENTRICLE; HEART LEFT VENTRICLE FUNCTION; HEART PERFORMANCE; IMMUNOBLOTTING; MALE; MOUSE; NONHUMAN; PRIORITY JOURNAL; SURVIVAL;

ANIMALS; BENZIMIDAZOLES; CARDIOMYOPATHIES; DISEASE MODELS, ANIMAL; FEMALE; GENE EXPRESSION REGULATION; HEART VENTRICLES; HUMANS; LAMIN TYPE A; MALE; MAP KINASE SIGNALING SYSTEM; MICE; MICE, INBRED C57BL; MICE, TRANSGENIC; MITOGEN-ACTIVATED PROTEIN KINASE 1; MITOGEN-ACTIVATED PROTEIN KINASE 3; MUTATION;

EID: 84890371523     PISSN: 09646906     EISSN: 14602083     Source Type: Journal    
DOI: 10.1093/hmg/ddt387     Document Type: Article

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