Transgenic replacement of type V adenylyl cyclase identifies a critical mechanism of β-adrenergic receptor dysfunction in the G(αq) overexpressing mouse

FEBS Letters

Volumn 458, Issue 2, 1999, Pages 236-240

  Tepe, Nicole M ^a   Liggett, Stephen B ^a  

^a UNIVERSITY OF CINCINNATI COLLEGE OF MEDICINE   (United States)

Author keywords

Adrenergic receptor; Adenylyl cyclase; cAMP; Desensitization; Hypertrophy

Indexed keywords

ADENYLATE CYCLASE; BETA ADRENERGIC RECEPTOR; CYCLIC AMP; GUANINE NUCLEOTIDE BINDING PROTEIN; ISOENZYME;

ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL ACTIVATION; CONTROLLED STUDY; ENZYME ACTIVITY; GENE OVEREXPRESSION; HEART MUSCLE CELL; HEART MUSCLE CONTRACTILITY; MOUSE; MUSCLE HYPERTROPHY; NONHUMAN; PRIORITY JOURNAL; TRANSGENIC MOUSE;

ADENYLATE CYCLASE; ANIMALS; CARDIOMEGALY; CATALYSIS; DISEASE MODELS, ANIMAL; GTP-BINDING PROTEIN ALPHA SUBUNITS, GQ-G11; GTP-BINDING PROTEINS; MALE; MICE; MICE, TRANSGENIC; RECEPTORS, ADRENERGIC, BETA; SIGNAL TRANSDUCTION; VENTRICULAR FUNCTION;

ANIMALIA; MUS MUSCULUS;

EID: 0032874674     PISSN: 00145793     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0014-5793(99)01147-3     Document Type: Article

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