u-0126 and Cadaver

u-0126 has been researched along with Cadaver* in 1 studies

Other Studies

1 other study(ies) available for u-0126 and Cadaver

Article	Year
Hypernuclear acetylation in atherosclerotic lesions and activated vascular smooth muscle cells. Biochemical and biophysical research communications, 1999, Dec-20, Volume: 266, Issue:2 Recent studies have implicated acetylation of several nuclear proteins such as histones and p53 on their epsilon-portion of lysine residues in eukaryotic transcription. Here we raised a specific polyclonal antibody against epsilon-acetylated lysine. Using the antibody, we detected hypernuclear acetylation (HNA) in atherosclerotic vascular smooth muscle cells (VSMCs). Thrombin, a humoral factor known to cause activation and proliferation of VSMCs, strongly potentiated HNA in cultured VSMCs. MAP kinase pathway and a signal coactivator CREB binding protein (CBP) were involved in thrombin-induced HNA of VSMCs. Our results suggest that coactivators cooperating with signal-dependent transcription activators play an important role in atherosclerogenesis via HNA in VSMCs. Topics: Acetylation; Antibodies; Butadienes; Cadaver; Cells, Cultured; Coronary Artery Disease; CREB-Binding Protein; Enzyme Activation; Enzyme Inhibitors; Hemagglutinins; Humans; Immunohistochemistry; Lysine; Mitogen-Activated Protein Kinases; Muscle, Smooth, Vascular; Nitriles; Nuclear Proteins; Thrombin; Trans-Activators; Transfection	1999

Article

Year

Hypernuclear acetylation in atherosclerotic lesions and activated vascular smooth muscle cells.

Biochemical and biophysical research communications, 1999, Dec-20, Volume: 266, Issue:2

Recent studies have implicated acetylation of several nuclear proteins such as histones and p53 on their epsilon-portion of lysine residues in eukaryotic transcription. Here we raised a specific polyclonal antibody against epsilon-acetylated lysine. Using the antibody, we detected hypernuclear acetylation (HNA) in atherosclerotic vascular smooth muscle cells (VSMCs). Thrombin, a humoral factor known to cause activation and proliferation of VSMCs, strongly potentiated HNA in cultured VSMCs. MAP kinase pathway and a signal coactivator CREB binding protein (CBP) were involved in thrombin-induced HNA of VSMCs. Our results suggest that coactivators cooperating with signal-dependent transcription activators play an important role in atherosclerogenesis via HNA in VSMCs.

Topics: Acetylation; Antibodies; Butadienes; Cadaver; Cells, Cultured; Coronary Artery Disease; CREB-Binding Protein; Enzyme Activation; Enzyme Inhibitors; Hemagglutinins; Humans; Immunohistochemistry; Lysine; Mitogen-Activated Protein Kinases; Muscle, Smooth, Vascular; Nitriles; Nuclear Proteins; Thrombin; Trans-Activators; Transfection

1999