The DOI matches its Crossref record; 107 of the 107 references it cites were found in a registry or an index.
Emergence of a DNA-damage response network consisting of Fanconi anaemia and BRCA proteins
Abstract
Fanconi anaemia (FA) has recently become an attractive model to study breast cancer susceptibility (BRCA) genes, as three FA genes, FANCD1, FANCN and FANCJ, are identical to the BRCA genes BRCA2, PALB2 and BRIP1. Increasing evidence shows that FA proteins function as signal transducers and DNA-processing molecules in a DNA-damage response network. This network consists of many proteins that maintain genome integrity, including ataxia telangiectasia and Rad3 related protein (ATR), Bloom syndrome protein (BLM), and BRCA1. Now that the gene that is defective in the thirteenth and last assigned FA complementation group (FANCI) has been identified, I discuss what is known about FA proteins and their interactive network, and what remains to be discovered.
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“FA is a rare cancer-prone disease in which patients’ cells are characterized by extreme sensitivity to agents that induce DNA interstrand crosslinks (for review, see [22,23]).”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [23]
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ATM and ATR Substrate Analysis Reveals Extensive Protein Networks Responsive to DNA Damage
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Hallmarks of 'BRCAness' in sporadic cancers
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Interaction of the Fanconi Anemia Proteins and BRCA1 in a Common Pathway
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Biallelic Inactivation of BRCA2 in Fanconi Anemia
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Embryonic lethality and radiation hypersensitivity mediated by Rad51 in mice lacking Brca2
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PALB2, which encodes a BRCA2-interacting protein, is a breast cancer susceptibility gene
Rahman, N., Seal, S., Thompson, D. J., Kelly, P. F., Renwick, A., Elliott, A., Reid, S., Spanova, K., Barfoot, R., Chagtai, T., et al. (2006) · Nature Genetics · doi:10.1038/ng1959 · Cited by 1,026
BRCA2 Is Required for Homology-Directed Repair of Chromosomal Breaks
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Control of BRCA2 Cellular and Clinical Functions by a Nuclear Partner, PALB2
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Metadata
- Authors
- Wang, W.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Wang, Weidong
- ORCID
- Wang, Weidong
- Venue
- Nature Reviews Genetics
- Published
- 2007-10
- Volume
- 8
- Issue
- 10
- Pages
- 735-748
- ISSN
- 1471-0056 (ISSN-L)
- 1471-0064
- OpenAlex
- W2010216792
- Cited by
- 663
- References
- 107
- Citations by year
- 2026: 6 · 2025: 9 · 2024: 11 · 2023: 5 · 2022: 15 · 2021: 10 · 2020: 17 · 2019: 20 · 2018: 12 · 2017: 28 · 2016: 24 · 2015: 31 · 2014: 40 · 2013: 52 · 2012: 52
- FWCI
- 6.87
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature Reviews Genetics (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
- Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
- Keywords
- Fanconi anemia, BRCA genes, DNA damage response, genome stability, BRCA2, FANCJ, FANCI, PALB2, BRIP1, ATR, Bloom syndrome protein, BRCA1, signal transduction, DNA repair, breast cancer susceptibility
- MeSH terms
- Fanconi Anemia Complementation Group N Protein, Animals, Chromatin, DNA, DNA Damage, DNA Repair, DNA-Binding Proteins, Fanconi Anemia, Humans, Nuclear Proteins, Signal Transduction, RNA Helicases, BRCA2 Protein, Tumor Suppressor Proteins, Ubiquitin-Protein Ligases, Fanconi Anemia Complementation Group Proteins
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