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

Chronic activation of G q coupled receptors, or overexpression of G αq, in cardiomyocytes results in hypertrophy, enhanced expression of fetal genes, decreased basal and β-adrenergic receptor (βAR) stimulated adenylyl cyclase (AC) activities, and depressed cardiac contractility in vivo. Among severa...

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Veröffentlicht in:	FEBS letters 1999-09, Vol.458 (2), p.236-240
Hauptverfasser:	Tepe, Nicole M, Liggett, Stephen B
Format:	Artikel
Sprache:	eng
Schlagworte:	ACV/Gαq, heterozygous crosses of transgenic mice overexpressing Gαq and type V adenylyl cyclase Adenylyl cyclase Adenylyl Cyclase Inhibitors Adenylyl Cyclases - genetics Adenylyl Cyclases - metabolism ANF, atrial natriuretic factor Animals cAMP Cardiomegaly - enzymology Cardiomegaly - genetics Cardiomegaly - pathology Catalysis Desensitization Disease Models, Animal GTP-Binding Protein alpha Subunits, Gq-G11 GTP-Binding Proteins - biosynthesis GTP-Binding Proteins - genetics Gαq, α subunit of the Gq guanine nucleotide binding protein Hypertrophy Male Mice Mice, Transgenic Receptors, Adrenergic, beta - physiology Signal Transduction - genetics Ventricular Function - genetics β-Adrenergic receptor βAR, β-adrenergic receptor
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