Biological and biochemical consequences of the human ERCC-1 repair gene after transfection into a repair-deficient CHO cell line.
The consequences of the presence of the human gene ERCC1 in repair-deficient 43-3B cells were examined. The gene restores the sensitivity of this mutant not only to UV but also to 4NQO, N-Ac-AAF and alkylating agents to the normal level. Also, the frequency of mutation induction by UV at the Na+/K+-ATPase locus returns to the level of CHO wild-type cells. Additionally, the rate of cyclobutane pyrimidine dimer removal approaches that in wild-type CHO cells. The results obtained indicate that the human gene ERCC-1 restores the impaired functions in 43-3B, and that the gene is probably functionally homologous to the defective one in the 43-3B cell line. Some evidence was found for a difference between the human gene product and its rodent counterpart, as the restoration of normal sensitivity to 4NQO, ENU and N-Ac-AAF was complete whereas it was not for UV.
D015112:4-Nitroquinoline-1-oxide / Q000494:pharmacology; D000099:Acetoxyacetylaminofluorene / Q000494:pharmacology; D000818:Animals; D002460:Cell Line; D006224:Cricetinae; D003412:Cricetulus; D004260:DNA Repair / Q000187:drug effects / Q000528:radiation effects; D005038:Ethylnitrosourea / Q000494:pharmacology; D006801:Humans; D009154:Mutation; D011740:Pyrimidine Dimers / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000235:genetics; D014170:Transformation, Genetic; D014466:Ultraviolet Rays
D011740:Pyrimidine Dimers; D015112:4-Nitroquinoline-1-oxide; D000099:Acetoxyacetylaminofluorene; D000254:Sodium-Potassium-Exchanging ATPase; D005038:Ethylnitrosourea