The DOI matches its Crossref record; 58 of the 61 references it cites were found in a registry or an index.
BACH1, a Novel Helicase-like Protein, Interacts Directly with BRCA1 and Contributes to Its DNA Repair Function
Open accessAbstract
BRCA1 interacts in vivo with a novel protein, BACH1, a member of the DEAH helicase family. BACH1 binds directly to the BRCT repeats of BRCA1. A BACH1 derivative, bearing a mutation in a residue that was essential for catalytic function in other helicases, interfered with normal double-strand break repair in a manner that was dependent on its BRCA1 binding function. Thus, BACH1/BRCA1 complex formation contributes to a key BRCA1 activity. In addition, germline BACH1 mutations affecting the helicase domain were detected in two early-onset breast cancer patients and not in 200 matched controls. Thus, it is conceivable that, like BRCA1, BACH1 is a target of germline cancer-inducing mutations.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source says what the claim attributes to it.
In the citing paper
“In particular, overexpression of the helicase-inactive K52R mutant in cells with wild-type FANCJ resulted in the accumulation of unrepaired DNA breaks when analyzed by pulse field electrophoresis [8], as well as reduced homologous recombination following double strand break induction [69].”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [8]
In the citing paper
“The purified 130-kDa protein was subject to tandem mass spectrometry and the FANCJ gene was cloned and found to consist of 20 exons spanning greater than 180 kb of genomic sequence in chromosome 17q22.”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [8]
In the citing paper
“Furthermore, unlike the classic paradigm for tumor suppressor genes, in which the tumor exclusively lacks the wild-type allele, tumors of individuals who were heterozygous for these two germline FANCJ mutations did not show loss of the corresponding wild-type allele [8].”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [8]
In the citing paper
“For example, the P47A variant identified in 2001 [8] and shown to disrupt FANCJ enzyme function [56] was found in the controls of a subsequent study and considered to be unrelated to breast cancer [44].”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [8]
In the citing paper
“Among the proteins identified was a protein of approximately 130 kDa that failed to interact with a BRCA1, harboring patient mutations within the BRCT motifs (P1749R and M1775R) [8].”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [8]
In the citing paper
“Most notably, the protein product had strong homology to the catalytic and nucleotide-binding domains of other members within the DEAH helicase family, including the xeroderma pigmentosum complimenting group D (XPD) [8].”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [8]
In the citing paper
“In keeping with this suggestion, two patients with a family history and early-onset breast cancer were identified that had discrete germline sequence changes, P47A and M299I, targeting the helicase domain of FANCJ [8].”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [8]
In the citing paper
“Moreover, the aforementioned P47A mutant had a reduced protein half-life when overexpressed in tissue culture cells [8].”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [8]
In the citing paper
“BRCA1 clinical mutations target the BRCT region required for FANCJ binding [8].”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [8]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Eng, J. K., McCormack, A. L., & Yates, J. R. (1994) · Journal of the American Society for Mass Spectrometry · doi:10.1016/1044-0305(94)80016-2 · Cited by 6,484
A Strong Candidate for the Breast and Ovarian Cancer Susceptibility Gene BRCA1
Miki, Y., Swensen, J. J., Shattuck-Eidens, D. M., Futreal, P. A., Harshman, K., Tavtigian, S. V., Liu, Q., Cochran, C., Bennett, L. M., Ding, W., et al. (1994) · Science · doi:10.1126/science.7545954 · Cited by 6,069
High-Efficiency Transformation of Mammalian Cells by Plasmid DNA
Chen, C., & Okayama, H. (1987) · Molecular and Cellular Biology · doi:10.1128/mcb.7.8.2745 · Cited by 5,327
Association of BRCA1 with Rad51 in Mitotic and Meiotic Cells
Scully, R., Chen, J., Plug, A., Xiao, Y., Weaver, D., Feunteun, J., Ashley, T., & Livingston, D. M. (1997) · Cell · doi:10.1016/s0092-8674(00)81847-4 · Cited by 1,459
Self-citationBrca1 Controls Homology-Directed DNA Repair
Moynahan, M. E., Chiu, J. W., Koller, B. H., & Jasin, M. (1999) · Molecular Cell · doi:10.1016/s1097-2765(00)80202-6 · Cited by 1,245
Carney, J. P., Maser, R. S., Olivares, H., Davis, E. M., Le Beau, M., Yates, J. R., Hays, L., Morgan, W. F., & Petrini, J. H. J. (1998) · Cell · doi:10.1016/s0092-8674(00)81175-7 · Cited by 1,226
Wang, Y., Cortez, D., Yazdi, P., Neff, N., Elledge, S. J., & Qin, J. (2000) · Genes & Development · doi:10.1101/gad.14.8.927 · Cited by 1,221
Stewart, G. S., Maser, R. S., Stankovic, T., Bressan, D. A., Kaplan, M. I., Jaspers, N. G. J., Raams, A., Byrd, P. J., Petrini, J. H. J., & Taylor, A. M. R. (1999) · Cell · doi:10.1016/s0092-8674(00)81547-0 · Cited by 1,060
Eckner, R., Ewen, M. E., Newsome, D., Gerdes, M., DeCaprio, J. A., Lawrence, J. B., & Livingston, D. M. (1994) · Genes & Development · doi:10.1101/gad.8.8.869 · Cited by 1,045
Self-citationDynamic changes of BRCA1 subnuclear location and phosphorylation state are initiated by DNA damage
Scully, R., Chen, J., Ochs, R. L., Keegan, K., Hoekstra, M., Feunteun, J., & Livingston, D. M. (1997) · Cell · doi:10.1016/s0092-8674(00)80503-6 · Cited by 900
Self-citation
Research works printed but not linked: 1
- Ma, 1994, Mutational analysis of ERCC3, which is involved in DNA repair and transcription initiation, Mol. Cell. Biol., 14, 4126, 10.1128/MCB.14.6.4126 · DOI
Cited by
Sorted by citations
Cancer Susceptibility and the Functions of BRCA1 and BRCA2
Venkitaraman, A. R. (2002) · Cell · doi:10.1016/s0092-8674(02)00615-3 · Cited by 1,713
BRCA1 and BRCA2: different roles in a common pathway of genome protection
Roy, R., Chun, J., & Powell, S. N. (2011) · Nature reviews. Cancer · doi:10.1038/nrc3181 · Cited by 1,555
BRCA1 and BRCA2: 1994 and beyond
Narod, S. A., & Foulkes, W. D. (2004) · Nature Reviews Cancer · doi:10.1038/nrc1431 · Cited by 967
Molecular views of recombination proteins and their control
West, S. C. (2003) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1127 · Cited by 977
Mitotic homologous recombination maintains genomic stability and suppresses tumorigenesis
Moynahan, M. E., & Jasin, M. (2010) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2851 · Cited by 959
Metadata
- Authors
- Cantor, S. B., Bell, D. W., Ganesan, S., Kass, E. M., Drapkin, R., Grossman, S., Wahrer, D. C. R., Sgroi, D. C., Lane, W. S., Haber, D. A., & Livingston, D. M.
- Affiliations
- Harvard University (US)
- Massachusetts General Hospital (US)
- Corresponding author
- Livingston, David M.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2001-04
- Volume
- 105
- Issue
- 1
- Pages
- 149-160
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2109173575
- Cited by
- 674
- References
- 61
- Citations by year
- 2026: 17 · 2025: 16 · 2024: 20 · 2023: 25 · 2022: 17 · 2021: 32 · 2020: 23 · 2019: 27 · 2018: 14 · 2017: 20 · 2016: 33 · 2015: 29 · 2014: 24 · 2013: 21 · 2012: 35
- FWCI
- 9.31
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- eScholarship@UMassChan (submittedVersion)
- Funders
- National Heart, Lung, and Blood Institute (T32HL007627, T32-HL07627-16)
- National Cancer Institute (P50 CA 89393, P50CA089393)
- 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, BRCA1, protein-protein interaction, DNA double-strand break repair, homologous recombination, germline mutations, early-onset breast cancer, cancer susceptibility genes
- MeSH terms
- Adult, Binding Sites, Boston, Breast Neoplasms, Cell Line, Chromosomes, Human, Pair 17, DNA Repair, DNA Helicases, DNA-Binding Proteins, Female, Genetic Testing, Humans, Molecular Sequence Data, Protein Binding, Recombinant Fusion Proteins, Transfection, Mutagenesis, Site-Directed, Sequence Homology, Amino Acid, Protein Structure, Tertiary, BRCA1 Protein, Genetic Predisposition to Disease, RNA Helicases, Amino Acid Motifs, Spectrometry, Mass, Electrospray Ionization, 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 ›
Are you an author, or do you see a problem with this page? Request a review
