Cardiac energy dependence on glucose activates metabolic genes controlled by mTOR

ABSTRACT: Mice lacking the expression of Acsl1 in the heart (Acsl1H-/-) have impaired cardiac fatty acid oxidation and develop spontaneous cardiac hypertrophy due to increased mTOR activation. To explore how the loss of ACSL1 alters gene expression, we performed a global gene expression analysis on ventricular RNA isolated from Acsl1H-/- and Acsl1flox/flox mice ten weeks after tamoxifen treatment when ACSL1 protein is completely lost and the specific activity of ACSL1 in Acsl1H-/- hearts is reduced 90%

ORGANISM(S): Mus musculus

PROVIDER: GSE51913 | GEO | 2014/09/29

SECONDARY ACCESSION(S): PRJNA225803

REPOSITORIES: GEO