ArticleNucleic acids research1991
Induction of a mutant phenotype in human repair proficient cells after overexpression of a mutated human DNA repair gene.
Article in Nucleic acids research, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Transcription-coupled repair of crosslinking DNA damage.DNA repair · 2025Review
- Mutational analysis of the human nucleotide excision repair gene ERCC1.Nucleic acids research · 1996Article
- Induction of Fanconi anemia cellular phenotype in human 293 cells by overexpression of a mutant FAC allele.The Journal of clinical investigation · 1996Article
- Specific inhibition of DNA polymerase beta by its 14 kDa domain: role of single- and double-stranded DNA binding and 5'-phosphate recognition.Nucleic acids research · 1995Article
- Studies on phenotypic complementation of ataxia-telangiectasia cells by chromosome transfer.American journal of human genetics · 1995Article
- Role of the human ERCC-1 gene in gene-specific repair of cisplatin-induced DNA damage.Nucleic acids research · 1994Article
- Messenger RNA levels of XPAC and ERCC1 in ovarian cancer tissue correlate with response to platinum-based chemotherapy.The Journal of clinical investigation · 1994Article
- Co-correction of the ERCC1, ERCC4 and xeroderma pigmentosum group F DNA repair defects in vitro.The EMBO journal · 1993Article
- Increased gene-specific repair of cisplatin interstrand cross-links in cisplatin-resistant human ovarian cancer cell lines.Molecular and cellular biology · 1992Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antisense and mutated cDNA of the human excision repair gene ERCC-1 were overexpressed in repair proficient HeLa cells by means of an Epstein-Barr-virus derived cDNA expression vector. Whereas antisense RNA did not influence the survival of the transfected cells, a mutated cDNA generating an ERCC-1 protein with two extra amino acids in a conserved region of its C-terminal part resulted in a significant sensitization of the HeLa transfectants to mitomycin C-induced damage. These results suggest that overexpression of the mutated ERCC-1 protein interferes with proper functioning of the excision repair pathway in repair proficient cells and is compatible with a model in which the mutated ERCC-1 protein competes with the wild-type polypeptide for a specific step in the repair process or for occupation of a site in a repair complex. Apparently, this effect is more pronounced for mitomycin C induced crosslink repair than for UV-induced DNA damage.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.