ArticleDNA repair2008
The Fanconi anemia core complex is required for efficient point mutagenesis and Rev1 foci assembly.
Article in DNA repair, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
59 citing papers in PubMed, 89 citations in OpenAlex.
- FANCA deficiency promotes leukaemic progression by allowing the emergence of cells carrying oncogenic driver mutations.Oncogene · 2023Article
- Safeguarding DNA Replication: A Golden Touch of MiDAS and Other Mechanisms.International journal of molecular sciences · 2022Review
- DNA damage and repair in the hematopoietic system.Acta biochimica et biophysica Sinica · 2022Review
- REV7 directs DNA repair pathway choice.Trends in cell biology · 2021Review
- The FANC/BRCA Pathway Releases Replication Blockades by Eliminating DNA Interstrand Cross-Links.Genes · 2020Review
- Review
- Biallelic inactivation of REV7 is associated with Fanconi anemia.The Journal of clinical investigation · 2016Article
- Involvement of translesion synthesis DNA polymerases in DNA interstrand crosslink repair.DNA repair · 2016Review
- A novel role for non-ubiquitinated FANCD2 in response to hydroxyurea-induced DNA damage.Oncogene · 2016Article
- The Regulation of DNA Damage Tolerance by Ubiquitin and Ubiquitin-Like Modifiers.Frontiers in genetics · 2016Review
- Chromosomal Integrity after UV Irradiation Requires FANCD2-Mediated Repair of Double Strand Breaks.PLoS genetics · 2016Article
- FANCD2 and REV1 cooperate in the protection of nascent DNA strands in response to replication stress.Nucleic acids research · 2015Article
- Fanconi anemia cells with unrepaired DNA damage activate components of the checkpoint recovery process.Theoretical biology & medical modelling · 2015Article
- Regulation of the Rev1-pol ζ complex during bypass of a DNA interstrand cross-link.The EMBO journal · 2015Article
- The structural basis of XRCC1-mediated DNA repair.DNA repair · 2015Review
- RNF4-mediated polyubiquitination regulates the Fanconi anemia/BRCA pathway.The Journal of clinical investigation · 2015Article
- The ADP-ribosyltransferase PARP10/ARTD10 interacts with proliferating cell nuclear antigen (PCNA) and is required for DNA damage tolerance.The Journal of biological chemistry · 2014Article
- A concomitant loss of dormant origins and FANCC exacerbates genome instability by impairing DNA replication fork progression.Nucleic acids research · 2014Article
- The carboxyl terminus of FANCE recruits FANCD2 to the Fanconi Anemia (FA) E3 ligase complex to promote the FA DNA repair pathway.The Journal of biological chemistry · 2014Article
- Mismatch repair protein MSH2 regulates translesion DNA synthesis following exposure of cells to UV radiation.Nucleic acids research · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Fanconi anemia (FA) is a chromosome instability syndrome characterized by congenital abnormalities, cellular hypersensitivity to DNA crosslinking agents, and heightened cancer risk. Eight of the thirteen identified FA genes encode subunits of a nuclear FA core complex that monoubiquitinates FANCD2 and FANCI to maintain genomic stability in response to replication stress. The FA pathway has been implicated in the regulation of error-prone DNA damage tolerance via an undefined molecular mechanism. Here, we show that the FA core complex is required for efficient spontaneous and UVC-induced point mutagenesis, independently of FANCD2 and FANCI. Consistent with the observed hypomutability of cells deficient in the FA core complex, we also demonstrate that these cells are impaired in the assembly of the error-prone translesion DNA synthesis polymerase Rev1 into nuclear foci. Consistent with a role downstream of the FA core complex and like known FA proteins, Rev1 is required to prevent DNA crosslinker-induced chromosomal aberrations in human cells. Interestingly, proliferating cell nuclear antigen (PCNA) monoubiquitination, known to contribute to Rev1 recruitment, does not require FA core complex function. Our results suggest a role for the FA core complex in regulating Rev1-dependent DNA damage tolerance independently of FANCD2, FANCI, and PCNA monoubiquitination.
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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.