ArticleBiochemistry2011
Impact of BRCA1 BRCT domain missense substitutions on phosphopeptide recognition.
Article in Biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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
30 citing papers in PubMed, 53 citations in OpenAlex.
- Domain-Specific Computational, Functional and Structural Methods Enable Interpretation ofCurrent oncology (Toronto, Ont.) · 2026Article
- Finding novel vulnerabilities of hypomorphic BRCA1 alleles.Molecular oncology · 2026Article
- PARP4 ADP-ribosylates PIDD1 to complete a phospho/SUMO/PAR-ylation cascade that orchestrates PIDDosome assembly.Science advances · 2026Article
- Triple-Action Therapy: Combining Machine Learning, Docking, and Dynamics to Combat BRCA1-Mutated Breast Cancer.Molecular biotechnology · 2025Article
- Hidden SVA retrotransposon insertion in BRCA1 revealed by nanopore targeted sequencing causes hereditary breast and ovarian cancer.Journal of human genetics · 2025Article
- Profiling BRCA1-BRCT interactions and their functional relevance at amino acid resolution.Nucleic acids research · 2025Article
- The Possible Mechanistic Basis of Individual Susceptibility to Spike Protein Injury.Advances in virology · 2025Review
- Protein-folding chaperones predict structure-function relationships and cancer risk in BRCA1 mutation carriers.Cell reports · 2024Article
- Double Heterozygosity for Rare Deleterious Variants in theInternational journal of molecular sciences · 2023Article
- Article
- Assessment of small in-frame indels and C-terminal nonsense variants of BRCA1 using a validated functional assay.Scientific reports · 2022Article
- Screening and identification of phytochemical drug molecules against mutant BRCA1 receptor of breast cancer using computational approaches.Molecular and cellular biochemistry · 2022Article
- InInternational journal of molecular sciences · 2021Article
- Fanconi anemia pathway as a prospective target for cancer intervention.Cell & bioscience · 2020Review
- Biophysical evaluation to categorize pathogenicity of cancer-predisposing mutations identified in the BARD1 BRCT domain.RSC advances · 2018Article
- A Novel Germline Mutation inJournal of breast cancer · 2017Article
- Clinically Significant Unclassified Variants inCancer research and treatment · 2017Article
- Recent discoveries in the molecular pathogenesis of the inherited bone marrow failure syndrome Fanconi anemia.Blood reviews · 2017Review
- Structure of BRCA1-BRCT/Abraxas Complex Reveals Phosphorylation-Dependent BRCT Dimerization at DNA Damage Sites.Molecular cell · 2016Article
- "DNA Binding Region" of BRCA1 Affects Genetic Stability through modulating the Intra-S-Phase Checkpoint.International journal of biological sciences · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The BRCA1 BRCT domain binds pSer-x-x-Phe motifs in partner proteins to regulate the cellular response to DNA damage. Approximately 120 distinct missense variants have been identified in the BRCA1 BRCT through breast cancer screening, and several of these have been linked to an increased cancer risk. Here we probe the structures and peptide-binding activities of variants that affect the BRCA1 BRCT phosphopeptide-binding groove. The results obtained from the G1656D and T1700A variants illustrate the role of Ser1655 in pSer recognition. Mutations at Arg1699 (R1699W and R1699Q) significantly reduce peptide binding through loss of contacts to the main chain of the Phe(+3) residue and, in the case of R1699W, to a destabilization of the BRCT fold. The R1835P and E1836K variants do not dramatically reduce peptide binding, in spite of the fact that these mutations significantly alter the structure of the walls of the Phe(+3) pocket.
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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.