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Gupta, Mahesh P.
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Gupta, Mahesh P.
Concurrent opposite effects of trichostatin A, an inhibitor of histone deacetylases, on expression of alpha-MHC and cardiac tubulins: implication for gain in cardiac muscle contractility.
SIRT3 is a stress-responsive deacetylase in cardiomyocytes that protects cells from stress-mediated cell death by deacetylation of Ku70.
SIRT1 promotes cell survival under stress by deacetylation-dependent deactivation of poly(ADP-ribose) polymerase 1.
HDAC3-dependent reversible lysine acetylation of cardiac myosin heavy chain isoforms modulates their enzymatic and motor activity.
Pathogenic properties of the N-terminal region of cardiac myosin binding protein-C in vitro.
The deacetylase SIRT1 promotes membrane localization and activation of Akt and PDK1 during tumorigenesis and cardiac hypertrophy.
The sirtuin SIRT6 blocks IGF-Akt signaling and development of cardiac hypertrophy by targeting c-Jun.
Acetylation of a conserved lysine residue in the ATP binding pocket of p38 augments its kinase activity during hypertrophy of cardiomyocytes.
SIRT3 deacetylates and activates OPA1 to regulate mitochondrial dynamics during stress.
Honokiol blocks and reverses cardiac hypertrophy in mice by activating mitochondrial Sirt3.
Obesity-induced lysine acetylation increases cardiac fatty acid oxidation and impairs insulin signalling.
Histone Deacetylase 3 (HDAC3)-dependent Reversible Lysine Acetylation of Cardiac Myosin Heavy Chain Isoforms Modulates Their Enzymatic and Motor Activity.
SIRT3 Blocks Aging-Associated Tissue Fibrosis in Mice by Deacetylating and Activating Glycogen Synthase Kinase 3?.
SIRT2 regulates oxidative stress-induced cell death through deacetylation of c-Jun NH2-terminal kinase.
Blocking cardiac toxicity of anticancer drugs