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One or more keywords matched the following properties of Gupta, Mahesh P.
overview Primary focus of my lab is to understand the molecular basis of heart failure, particularly, the role played by the chromatin remodeling enzymes in muscle gene regulation, cellular senescence and cardiac hypertrophy and fibrosis. Heart failure is a pathological state in which the heart is unable to pump blood at a rate commensurate with requirements of the metabolizing tissues. It is usually caused by a defect in myocardial contraction. Reduced myocardial contractile function may reflect a decrease in number of viable myocytes, dysfunction of viable myocytes, or alterations to the intrinsic contractile activity of individual myocytes. At the molecular level, several abnormalities have been observed, including alterations in the expression of numerous genes that are central to the normal structure and function of the heart; however, the basic mechanism of heart failure is not yet fully understood. With recent advancements in cell biology, it has become clear that factors modifying chromatin structure, e.g. histone deacetylases, acetyltransferases and sirtuins play a fundamental role in this process. In addition to modifying chromatin structure, these enzymes also play a role out side the nucleus. We are trying to understand how these enzymes modify mitochondrial proteins and regulate the cell-survivability and contractile function, in response to various pathophysiological stresses, including obesity/diabetes, hemodynamic overloads and aging.
One or more keywords matched the following items that are connected to Gupta, Mahesh P.
Item TypeName
Concept Histone Deacetylases
Concept Histone Demethylases
Concept Histone Deacetylase Inhibitors
Academic Article Calcium/calmodulin-dependent protein kinase activates serum response factor transcription activity by its dissociation from histone deacetylase, HDAC4. Implications in cardiac muscle gene regulation during hypertrophy.
Academic Article Poly(ADP-ribose) polymerase-1-dependent cardiac myocyte cell death during heart failure is mediated by NAD+ depletion and reduced Sir2alpha deacetylase activity.
Academic Article 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.
Academic Article HDAC4 and PCAF bind to cardiac sarcomeres and play a role in regulating myofilament contractile activity.
Academic Article SIRT3 is a stress-responsive deacetylase in cardiomyocytes that protects cells from stress-mediated cell death by deacetylation of Ku70.
Academic Article Dephosphorylation and caspase processing generate distinct nuclear pools of histone deacetylase 4.
Academic Article HDAC3-dependent reversible lysine acetylation of cardiac myosin heavy chain isoforms modulates their enzymatic and motor activity.
Academic Article The sirtuin SIRT6 blocks IGF-Akt signaling and development of cardiac hypertrophy by targeting c-Jun.
Academic Article Activation of SIRT1, a class III histone deacetylase, contributes to fructose feeding-mediated induction of the alpha-myosin heavy chain expression.
Academic Article Acetylation of a conserved lysine residue in the ATP binding pocket of p38 augments its kinase activity during hypertrophy of cardiomyocytes.
Academic Article Histone Deacetylase 3 (HDAC3)-dependent Reversible Lysine Acetylation of Cardiac Myosin Heavy Chain Isoforms Modulates Their Enzymatic and Motor Activity.
Academic Article The histone deacetylase SIRT6 blocks myostatin expression and development of muscle atrophy.
Grant Histone deacetylases in pathogenesis of heart failure
Grant The Role of PARP-SIR2 Signaling in Heart Failure
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  • Histones