Activation of cytochrome P450IA1 gene expression by 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin in wild-type and high-activity variant mouse hepatoma cells

1989 ◽  
Vol 2 (1) ◽  
pp. 40-46 ◽  
Author(s):  
Margaret A. Hirst ◽  
Keith W. Jones ◽  
James P. Whitlock
Keyword(s):  
Gene Expression ◽  
High Activity ◽  
Hepatoma Cells ◽  
Wild Type ◽  
Mouse Hepatoma ◽  
Tetrachlorodibenzo P Dioxin

Generation and characterization of variants of mouse hepatoma cells with defects in hepato-specific gene expression. I. Albumin synthesis variants

1982 ◽  
Vol 8 (4) ◽  
pp. 451-464 ◽  
Author(s):  
Gretchen J. Darlington ◽  
John Papaconstantinou ◽  
David W. Sammons ◽  
Peter C. Brown ◽  
Edith Y. Wong ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hepatoma Cells ◽  
Specific Gene ◽  
Albumin Synthesis ◽  
Specific Gene Expression ◽  
Mouse Hepatoma

Downregulation of the Ah receptor in mouse hepatoma cells treated in culture with 2,3,7,8-tetrachlorodibenzo-p-dioxin

1991 ◽  
Vol 69 (8) ◽  
pp. 1204-1210 ◽  
Author(s):  
Rebecca D. Prokipcak ◽  
Allan B. Okey
Keyword(s):  
Nuclear Receptor ◽  
Specific Binding ◽  
Hepatoma Cells ◽  
Ah Receptor ◽  
Short Term ◽  
Mouse Hepatoma ◽  
Receptor Sites ◽  
Short Term Exposure ◽  
Cytosolic Extract ◽  
Tetrachlorodibenzo P Dioxin

The aromatic hydrocarbon (Ah) receptor behaves as a ligand-dependent transcription factor in the induction of cytochrome P450IA1. In cells exposed to the Ah receptor ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the Ah receptor undergoes a transformation from a form with low affinity for nucleic acids (cytosolic receptor) into a form that preferentially associates with the cell nucleus (nuclear receptor). We followed the fate of the Ah receptor in mouse hepatoma cells during short-term exposure to [3H]TCDD by analyzing both cytosolic and nuclear fractions for specific binding. Nuclear Ah receptor levels increased over the first 2 h of treatment and then decreased to about 50% of maximal concentrations by 5 h after start of treatment. The decrease in nuclear receptor was not accompanied by a reappearance of detectable Ah receptor in the cytosolic fraction; further incubation with [3H]TCDD in cytosols from lysed cells did not label any additional receptor sites in cytosolic extract. By the 6th h of incubation, the total receptor population in the cell was only about 15–20% of that detected at the start of the incubation. The levels of specific binding detected were unaffected by up to 20 h of incubation with the vehicle DMSO, confirming that the presence of TCDD is required for the observed downregulation to occur. These results indicate that there is a substantial ligand-dependent loss in total Ah receptor during short-term exposure of cells to TCDD in culture.Key words: Ah receptor, 2,3,7,8-tetrachlorodibenzo-p-dioxin, dioxin toxicity, Hepa-1 mouse hepatoma cells.

scholarly journals Wild-type function of the p53 tumor suppressor protein is not required for apoptosis of mouse hepatoma cells

1998 ◽  
Vol 5 (1) ◽  
pp. 87-95 ◽  
Author(s):  
Christina Unger ◽  
Albrecht Buchmann ◽  
Christoph L Bünemann ◽  
Stefan Kress ◽  
Michael Schwarz
Keyword(s):  
Tumor Suppressor ◽  
Hepatoma Cells ◽  
Tumor Suppressor Protein ◽  
Wild Type ◽  
Type Function ◽  
P53 Tumor Suppressor ◽  
Mouse Hepatoma ◽  
P53 Tumor Suppressor Protein

scholarly journals Oxygen- and dioxin-regulated gene expression in mouse hepatoma cells

1997 ◽  
Vol 51 (2) ◽  
pp. 567-574 ◽  
Author(s):  
Max Gassmann ◽  
Ivica Kvietikova ◽  
Andreas Rolfs ◽  
Roland H. Wenger
Keyword(s):  
Gene Expression ◽  
Hepatoma Cells ◽  
Mouse Hepatoma ◽  
Regulated Gene Expression

Influence of aryl hydrocarbon- (Ah) receptor and genotoxins on DNA repair gene expression and cell survival of mouse hepatoma cells

Toxicology ◽  
2009 ◽  
Vol 259 (3) ◽  
pp. 91-96 ◽  
Author(s):  
Ilona Schreck ◽  
Doreen Chudziak ◽  
Sandra Schneider ◽  
Albrecht Seidel ◽  
Karl L. Platt ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Repair ◽  
Cell Survival ◽  
Hepatoma Cells ◽  
Ah Receptor ◽  
Repair Gene ◽  
Aryl Hydrocarbon ◽  
Mouse Hepatoma ◽  
Dna Repair Gene
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