The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.
Identification of KIAA1018/FAN1, a DNA Repair Nuclease Recruited to DNA Damage by Monoubiquitinated FANCD2
Open accessAbstract
SUMMARY DNA interstrand crosslinks (ICLs) are highly toxic because they block the progression of replisomes. The Fanconi Anemia (FA) proteins, encoded by genes that are mutated in FA, are important for repair of ICLs. The FA core complex catalyzes the monoubiquitination of FANCD2, and this event is essential for several steps of ICL repair. However, how monoubiquitination of FANCD2 promotes ICL repair at the molecular level is unknown. Here, we describe a highly conserved protein, KIAA1018/MTMR15/FAN1, that interacts with, and is recruited to sites of DNA damage by, the monoubiquitinated form of FANCD2. FAN1 exhibits endonuclease activity toward 5′ flaps and has 5′ exonuclease activity, and these activities are mediated by an ancient VRR_nuc domain. Depletion of FAN1 from human cells causes hypersensitivity to ICLs, defects in ICL repair, and genome instability. These data at least partly explain how ubiquitination of FANCD2 promotes DNA repair.
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Cites
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Ubiquitin-binding domains in Y-family polymerases regulate translesion synthesis.
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Self-citationIdentification of the FANCI Protein, a Monoubiquitinated FANCD2 Paralog Required for DNA Repair
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Self-citationEmergence of a DNA-damage response network consisting of Fanconi anaemia and BRCA proteins
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The Fanconi Anemia Pathway Promotes Replication-Dependent DNA Interstrand Cross-Link Repair
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Cited by
The DNA Damage Response: Making It Safe to Play with Knives
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Identification of Genetic Factors that Modify Clinical Onset of Huntington’s Disease
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“The FAN1 nuclease plays a role in repair of DNA inter-strand cross-links but not of double-strand breaks (Kratz et al., 2010; Liu et al., 2010; MacKay et al., 2010) and has recently been identified as essential for restart of paused replication forks in DNA synthesis (Chaudhury et al.”
CAG Repeat Not Polyglutamine Length Determines Timing of Huntington’s Disease Onset
Lee, J.-M., Correia, K., Loupe, J., Kim, K.-H., Barker, D., Hong, E. P., Chao, M. J., Long, J. D., Lucente, D., Vonsattel, J. P. G., et al. (2019) · Cell · doi:10.1016/j.cell.2019.06.036 · Cited by 538
Regulation of DNA cross-link repair by the Fanconi anemia/BRCA pathway
Kim, H., & D'Andrea, A. D. (2012) · Genes & Development · doi:10.1101/gad.195248.112 · Cited by 508
Metadata
- Authors
- MacKay, C., Déclais, A.-C., Lundin, C., Agostinho, A., Deans, A. J., MacArtney, T. J., Hofmann, K., Gartner, A., West, S. C., Helleday, T., Lilley, D. M. J., & Rouse, J.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2010-07
- Volume
- 142
- Issue
- 1
- Pages
- 65-76
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2159859860
- Cited by
- 313
- References
- 33
- FWCI
- 13.47
- Type
- journal article
- Language
- en
- Open access
- bronze
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- MacKay, C., Déclais, A.-C., Lundin, C., Agostinho, A., Deans, A. J., MacArtney, T. J., Hofmann, K., Gartner, A., West, S. C., Helleday, T., Lilley, D. M. J., & Rouse, J. (2010). Identification of KIAA1018/FAN1, a DNA Repair Nuclease Recruited to DNA Damage by Monoubiquitinated FANCD2. Cell. https://doi.org/10.1016/j.cell.2010.06.021
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