Cyclin kinase inhibitor p21 potentiates bile acid–induced apoptosis in hepatocytes that is dependent on p53

Prolonged activation of the mitogen-activated protein kinase (MAPK) pathway enhances expression of the cyclin kinase inhibitor p21 that can promote growth arrest and cell survival in response to cytotoxic insults. Bile acids can also cause prolonged MAPK activation that is cytoprotective against bil...

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Veröffentlicht in:	Hepatology (Baltimore, Md.) Md.), 2002-07, Vol.36 (1), p.39-48
Hauptverfasser:	Qiao, Liang, McKinstry, Robert, Gupta, Seema, Gilfor, Donna, Windle, Jolene J., Hylemon, Philip B., Grant, Steven, Fisher, Paul B., Dent, Paul
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Apoptosis - drug effects Bile Acids and Salts - pharmacology Biological and medical sciences Blotting, Western Caspase 3 Caspases - metabolism Cells, Cultured Cyclin-Dependent Kinase Inhibitor p21 Cyclins - deficiency Cyclins - genetics Cyclins - physiology Deoxycholic Acid - pharmacology Drug Synergism Electrophoresis, Polyacrylamide Gel Enzyme Activation - drug effects Enzyme Precursors - metabolism Fundamental and applied biological sciences. Psychology Gene Expression Hepatocytes - cytology Hepatocytes - drug effects Hepatocytes - metabolism In Situ Nick-End Labeling Liver. Bile. Biliary tracts Male Mice Mice, Inbred C57BL Mice, Knockout Mitogen-Activated Protein Kinases - metabolism Receptor, Epidermal Growth Factor - metabolism Signal Transduction - drug effects Transfection Tumor Suppressor Protein p53 - physiology Vertebrates: digestive system
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