Using a gene-switch transgenic approach to dissect distinct roles of MAP kinases in heart failure

Cold Spring Harbor Symposia on Quantitative Biology

Volumn 67, Issue , 2002, Pages 429-437

  Petrich, B G ^a   Liao, P ^a,b   Wang, Y ^a  

^a UNIVERSITY OF MARYLAND SCHOOL OF MEDICINE   (United States)

^b UNIVERSITY OF TORONTO   (Canada)

Author keywords

[No Author keywords available]

Indexed keywords

COLLAGEN; FIBRONECTIN; GENE PRODUCT; MITOGEN ACTIVATED PROTEIN KINASE; PROTEIN RAS; STRESS ACTIVATED PROTEIN KINASE; SYNAPTOPHYSIN; UNCLASSIFIED DRUG; MITOGEN ACTIVATED PROTEIN KINASE P38;

CALCIUM CELL LEVEL; CARDIOMYOPATHY; CELL COMMUNICATION; CELL INTERACTION; CONFERENCE PAPER; DISEASE ASSOCIATION; ENZYME ACTIVATION; ENZYME ACTIVITY; FIBROSING ALVEOLITIS; GENE CONTROL; GENE TARGETING; GENOME; HEART CONTRACTION; HEART FAILURE; HEART INFARCTION; HEART MUSCLE; HEART VENTRICLE HYPERTROPHY; MUSCLE FIBER CONTRACTION; PATHOPHYSIOLOGY; PRIORITY JOURNAL; PROTEIN EXPRESSION; SIGNAL TRANSDUCTION; STRESS; ARTICLE; DIASTOLIC DYSFUNCTION; GENE SWITCHING; GENETIC MANIPULATION; HEART CELL CULTURE; HEART HYPERTROPHY; HEART MUSCLE CONTRACTILITY; HEART VENTRICLE REMODELING; IN VITRO STUDY; IN VIVO STUDY; MUSCLE CELL; NONHUMAN; PROTEIN FUNCTION;

ANIMALIA;

EID: 0038143309     PISSN: 00917451     EISSN: None     Source Type: Book Series    
DOI: 10.1101/sqb.2002.67.429     Document Type: Conference Paper

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