BACH1 is critical for homologous recombination and appears to be the Fanconi anemia gene product FANCJ
Open accessAbstract
We showed in this study that cells deficient of the BRCA1-associated BACH1 helicase, also known as BRIP1, failed to elicit homologous recombination (HR) after DNA double-stranded breaks (DSBs). BACH1-deficient cells were also sensitive to mitomycin C (MMC) and underwent MMC-induced chromosome instability. Moreover, we identified a homozygous nonsense mutation in BACH1 in a FA-J patient-derived cell line and could not detect BACH1 protein in this cell line. Expression of wild-type BACH1 in this cell line reduced the accumulation of cells at G2/M phases following exposure to DNA crosslinkers, a characteristic of Fanconi anemia (FA) cells. These results support the conclusion that BACH1 is FANCJ.
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R798x is predicted to produce a truncated protein, but no detectable protein product was found.
“The R798x mutation predicts a truncated protein, but a detectable protein product was not found [26].”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [26]
The most common FANCJ germline mutant allele is R798x.
“Of all the FANCJ germline mutations, the most common mutant allele is FANCJ R798x.”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [26]
Bi-allelic mutations in BACH1/FANCJ/BRIP1 or PALB2/FANCN cause the FA subtypes FA-J or FA-N, respectively.
“Similarly, inheriting bi-allelic mutations in BACH1/FANCJ/ BRIP1 or PALB2/FANCN genes results in the FA subtypes FA-J or FA-N, respectively (Figure 1) [26–30].”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [26]
FANCJ mediates a subset of BRCA1 functions in double-strand break repair.
“Using a DNA double-strand break-induced recombination assay [75], siRNA depletion of FANCJ was shown to substantially [26] or partially reduce homologous recombination [38], supporting the idea that FANCJ mediates a subset of BRCA1 functions in double-strand break repair.”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [26]
siRNA depletion of FANCJ substantially or partially reduced homologous recombination.
“Using a DNA double-strand break-induced recombination assay [75], siRNA depletion of FANCJ was shown to substantially [26] or partially reduce homologous recombination [38], supporting the idea that FANCJ mediates a subset of BRCA1 functions in double-strand break repair.”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [26]
FANCJ may participate with BRCA1 in resolving stalled replication forks or crosslinked DNA, which would explain the extreme sensitivity and massive chromosomal rearrangements seen in FANCJ- and BRCA1-deficient cells after interstrand crosslink agents.
“Instead, FANCJ could participate with BRCA1 in a distinct aspect of DNA repair associated with resolving stalled replication forks or crosslinked DNA, a function that explains the extreme sensitivity and massive chromosomal rearrangements found in FANCJ- and BRCA1-deficient cells in response to agents that induce interstrand crosslinks [26].”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [26]
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Self-citation
- Authors
- Litman, R., Peng, M., Jin, Z., Zhang, F., Zhang, J., Powell, S., Andreassen, P. R., & Cantor, S. B.
- Affiliations
- University of Massachusetts Chan Medical School (US)
- Cincinnati Children's Hospital Medical Center (US)
- Washington University in St. Louis (US)
- Corresponding author
- Cantor, Sharon B.
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2005-09
- Volume
- 8
- Issue
- 3
- Pages
- 255-265
- ISSN
- 1535-6108 (ISSN-L)
- OpenAlex
- W2109630092
- Cited by
- 396
- References
- 58
- Citations by year
- 2026: 9 · 2025: 10 · 2024: 6 · 2023: 14 · 2022: 8 · 2021: 19 · 2020: 15 · 2019: 12 · 2018: 9 · 2017: 17 · 2016: 21 · 2015: 20 · 2014: 17 · 2013: 18 · 2012: 29
- FWCI
- 10.35
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion)
- Funders
- Mary Kay Foundation
- University of Massachusetts Medical School
- 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
- BACH1, BRIP1, FANCJ, Fanconi anemia, homologous recombination, DNA double-strand breaks, mitomycin C sensitivity, chromosomal instability, G2/M cell cycle arrest, nonsense mutation, helicase
- MeSH terms
- Breast Neoplasms, Cell Division, Chromosome Mapping, Fanconi Anemia, Female, Humans, Recombination, Genetic, Transcription Factors, Transfection, G2 Phase, Leucine Zippers, Genes, Reporter, DNA Primers, Cell Line, Tumor, Green Fluorescent Proteins, Basic-Leucine Zipper Transcription Factors, Fanconi Anemia Complementation Group Proteins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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