ArticleNucleic acids research2005
The BRCT domain of mammalian Rev1 is involved in regulating DNA translesion synthesis.
Article in Nucleic acids research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 87 citations in OpenAlex.
- Plasmodium falciparum DNA repair dynamics reveal unique roles for TLS polymerases and PfRad51 in genome diversification.Nucleic acids research · 2025Article
- REV1 coordinates a multi-faceted tolerance response to DNA alkylation damage and prevents chromosome shattering in Drosophila melanogaster.PLoS genetics · 2024Article
- Protein Assemblies in Translesion Synthesis.Genes · 2024Review
- Translesion synthesis polymerases are dispensable for C. elegans reproduction but suppress genome scarring by polymerase theta-mediated end joining.PLoS genetics · 2020Article
- DNA damage tolerance in stem cells, ageing, mutagenesis, disease and cancer therapy.Nucleic acids research · 2019Review
- Mutating for Good: DNA Damage Responses During Somatic Hypermutation.Frontiers in immunology · 2019Review
- The Rev1-Polζ translesion synthesis mutasome: Structure, interactions and inhibition.The Enzymes · 2019Review
- Inhibition of mutagenic translesion synthesis: A possible strategy for improving chemotherapy?PLoS genetics · 2017Review
- Article
- Rev1 is a base excision repair enzyme with 5'-deoxyribose phosphate lyase activity.Nucleic acids research · 2016Article
- FANCD2 and REV1 cooperate in the protection of nascent DNA strands in response to replication stress.Nucleic acids research · 2015Article
- Excision of translesion synthesis errors orchestrates responses to helix-distorting DNA lesions.The Journal of cell biology · 2015Article
- Starvation promotes REV1 SUMOylation and p53-dependent sensitization of melanoma and breast cancer cells.Cancer research · 2015Article
- Translesion DNA synthesis and mutagenesis in eukaryotes.Cold Spring Harbor perspectives in biology · 2013Review
- Defining a genotoxic profile with mouse embryonic stem cells.Experimental biology and medicine (Maywood, N.J.) · 2013Review
- Structure and functional analysis of the BRCT domain of translesion synthesis DNA polymerase Rev1.Biochemistry · 2013Article
- The vital role of polymerase ζ and REV1 in mutagenic, but not correct, DNA synthesis across benzo[a]pyrene-dG and recruitment of polymerase ζ by REV1 to replication-stalled site.The Journal of biological chemistry · 2012Article
- Translesion DNA synthesis in the context of cancer research.Cancer cell international · 2011Article
- Molecular chaperone Hsp90 regulates REV1-mediated mutagenesis.Molecular and cellular biology · 2011Article
- DNA polymerases and cancer.Nature reviews. Cancer · 2011Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rev1 is a deoxycytidyl transferase associated with DNA translesion synthesis (TLS). In addition to its catalytic domain, Rev1 possesses a so-called BRCA1 C-terminal (BRCT) domain. Here, we describe cells and mice containing a targeted deletion of this domain. Rev1(B/B) mice are healthy, fertile and display normal somatic hypermutation. Rev1(B/B) cells display an elevated spontaneous frequency of intragenic deletions at Hprt. In addition, these cells were sensitized to exogenous DNA damages. Ultraviolet-C (UV-C) light induced a delayed progression through late S and G2 phases of the cell cycle and many chromatid aberrations, specifically in a subset of mutant cells, but not enhanced sister chromatid exchanges (SCE). UV-C-induced mutagenesis was reduced and mutations at thymidine-thymidine dimers were absent in Rev1(B/B) cells, the opposite phenotype of UV-C-exposed cells from XP-V patients, lacking TLS polymerase eta. This suggests that the enhanced UV-induced mutagenesis in XP-V patients may depend on error-prone Rev1-dependent TLS. Together, these data indicate a regulatory role of the Rev1 BRCT domain in TLS of a limited spectrum of endogenous and exogenous nucleotide damages during a defined phase of the cell cycle.
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