PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 19124542-6 2009 In contrast, the phorbol ester PMA (phorbol-12-myristate-13-acetate, a pharmacological mimic of the downstream mediator diacylglycerol in alpha-adrenergic signalling), caused continuous PKD-dependent HDAC5-GFP nuclear efflux and maintained PKD1-mPlum redistribution. Tetradecanoylphorbol Acetate 36-67 protein kinase D1 Mus musculus 186-189 21047949-3 2011 In this study, we demonstrate that MA-10 mouse Leydig tumor cells express several PKC isoforms to varying levels and that the activation of PKC signaling, by phorbol 12-myristate 13-acetate (PMA) elevated the expression and phosphorylation of PKCalpha, -delta, -epsilon, and -mu/protein kinase D (PKD). Tetradecanoylphorbol Acetate 158-189 protein kinase D1 Mus musculus 297-300 21047949-3 2011 In this study, we demonstrate that MA-10 mouse Leydig tumor cells express several PKC isoforms to varying levels and that the activation of PKC signaling, by phorbol 12-myristate 13-acetate (PMA) elevated the expression and phosphorylation of PKCalpha, -delta, -epsilon, and -mu/protein kinase D (PKD). Tetradecanoylphorbol Acetate 191-194 protein kinase D1 Mus musculus 297-300 21047949-6 2011 PKD was capable of controlling PMA and cAMP/PKA-mediated synergism involved in the steroidogenic response. Tetradecanoylphorbol Acetate 31-34 protein kinase D1 Mus musculus 0-3 19124542-6 2009 In contrast, the phorbol ester PMA (phorbol-12-myristate-13-acetate, a pharmacological mimic of the downstream mediator diacylglycerol in alpha-adrenergic signalling), caused continuous PKD-dependent HDAC5-GFP nuclear efflux and maintained PKD1-mPlum redistribution. Tetradecanoylphorbol Acetate 31-34 protein kinase D1 Mus musculus 186-189 19124542-7 2009 In the absence of expressed HDAC, PMA increased histone H3 acetylation and increased MEF2 reporter activity in a PKD-dependent manner, consistent with PKD phosphorylation of endogenous HDAC(s) and reduced nuclear HDAC activity due to HDAC nuclear efflux. Tetradecanoylphorbol Acetate 34-37 protein kinase D1 Mus musculus 113-116 19124542-7 2009 In the absence of expressed HDAC, PMA increased histone H3 acetylation and increased MEF2 reporter activity in a PKD-dependent manner, consistent with PKD phosphorylation of endogenous HDAC(s) and reduced nuclear HDAC activity due to HDAC nuclear efflux. Tetradecanoylphorbol Acetate 34-37 protein kinase D1 Mus musculus 151-154 16098040-5 2005 Elevated extracellular calcium and acute 12-O-tetradecanoylphorbol-13-acetate (TPA) treatments induced differentiation and triggered a downmodulation of PKD levels, autophosphorylation at serine 916, and activity. Tetradecanoylphorbol Acetate 41-77 protein kinase D1 Mus musculus 153-156 16098040-5 2005 Elevated extracellular calcium and acute 12-O-tetradecanoylphorbol-13-acetate (TPA) treatments induced differentiation and triggered a downmodulation of PKD levels, autophosphorylation at serine 916, and activity. Tetradecanoylphorbol Acetate 79-82 protein kinase D1 Mus musculus 153-156 16098040-6 2005 Chronic TPA treatment stimulated proliferation and resulted in a recovery of PKD levels, autophosphorylation, and activity. Tetradecanoylphorbol Acetate 8-11 protein kinase D1 Mus musculus 77-80