Hankinson O. Single-step selection of clones of a mouse hepatoma line deficient in aryl hydrocarbon hydroxylase. Proc. Natl. Acad. Sci. USA 76: 373-376, 1979. PubMed: 106390
Legraverend C, et al. Regulatory gene product of the Ah locus. Characterization of receptor mutants among mouse hepatoma clones. J. Biol. Chem. 257: 6402-6407, 1987. PubMed: 6896205
Hoffman EC, et al. Cloning of a factor required for activity of the Ah (dioxin) receptor. Science 252: 954-958, 1991. PubMed: 1852076
Numayama-Tsuruta K, et al. A point mutation responsible for defective function of the aryl-hydrocarbon-receptor nuclear translocator in mutant Hepa-1c1c7 cells. Eur. J. Biochem. 246: 486-495, 1997. PubMed: 9208942
Hankinson OMutants of cultured hepatoma cells deficient in aryl hydrocarbon hydroxylaseIn: Hankinson OMicrosomes, drug oxidations, and chemical carcinogenesis2New YorkAcademic Presspp. 1149-1152, 1980
The c4 (B13NBii1) cell line was derived from Hepa-1c1c7 (ATCC CRL-2026). Hepa-1c1c7 has high aryl hydrocarbon hydroxylase (AHH) activity. The cells were exposed to N-methyl-N'-nitro-N- nitrosoguanidine (MNNG) and mutant colonies were selected for benzo[a]pyrene resistance. The c4 (B13NBii1) cell line lacks functional aryl hydrocarbon receptor nuclear translocator protein (ARNT), due to a point mutation (Gly-326 to Asp) in the ARNT gene. ARNT is directly involved in the regulation of xenobiotic metabolism (including chemical carcinogenesis), hypoxia and differentiation during embryogeneses. The parental cell line c4 (B13NBii1)(CRL-2717) lacks functional ARNT while its derivative vT{2} (CRL-2712) possesses a complete transfected ARNT cDNA. Together, they can be used to study ARNT processes and the role of ARNT in vivo.
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