| First Author | Kikuchi H | Year | 1994 |
| Journal | Jpn J Cancer Res | Volume | 85 |
| Issue | 7 | Pages | 710-7 |
| PubMed ID | 8071113 | Mgi Jnum | J:19825 |
| Mgi Id | MGI:67951 | Doi | 10.1111/j.1349-7006.1994.tb02419.x |
| Citation | Kikuchi H, et al. (1994) Aberrant CYP1A1 induction: discrepancy of CYP1A1 mRNA and aryl hydrocarbon hydroxylase activity in mutant cells of mouse hepatoma line, Hepa-1. Jpn J Cancer Res 85(7):710-7 |
| abstractText | We have isolated new benzo[a]pyrene-resistant clones, cl-21 and cl-32, of the mouse hepatoma line, Hepa-1. CYP1A1-dependent aryl hydrocarbon hydroxylase activity is not inducible by 2,3,7,8-tetrachlorodibenzo-p-dioxin or 3-methylcholanthrene in these two cell lines. However, mRNA of CYP1A1 is inducible in cl-21 and cl-32 cells, as in the wild-type cells, in spite of an undetectable level of cytosolic Ah receptor. The cl-21 cDNA of Cyp1a-1 was found to have a single mutation leading to an amino acid substitution from Leu (118) to Arg (118). However, the CYP1A1 protein band was not detected on Western immunoblots. The cDNA of cl-32 was found to have a single mutation leading to an amino acid change from Arg (359) to Trp (359). The presence of the mature protein in cl-32 was confirmed by Western blot analysis. Somatic cell hybridization experiments demonstrated that the phenotype of cl-21 and cl-32 is recessive and that these clones belong to the same complementation group. These data suggest that there may be a non-Ah receptor-mediated mechanism of CYP1A1 induction. |
