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We have studied PKC-mediated phosphorylation events in neonatal cardiac myocytes using back phosphorylation. 3 nM 4-β 12-myristate-13-acetate (PMA)-intact cell treatment preferentially activates PKC in these cells (Circ. Res. 76 (1995) 654) and caused decreased 32 P incorporation (back phosphorylation) into an ~18-kDa protein. This response required physiological levels of free Mg...
In the present study we characterized a ''crosstalk'' mechanism between transforming growth factor beta-1 (TGF β-1) and endothelin-1 (ET1) signaling pathways in neonatal cardiac myocytes. A 5 minute pretreatment with 1 ng/ml concentrations of TGF β-1 attenuated ET1-induced negative chronotropic effects and translocation of the α, δ and PKC isozymes to the particulate cell fraction. We found no effect...
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