ArticleCancer research2015
Interaction of BARD1 and HP1 Is Required for BRCA1 Retention at Sites of DNA Damage.
Article in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 99 citations in OpenAlex.
- ISWI/CHRAC orchestrates sequential chromatin-remodeling activities by mobilizing DNA polymerase ε for homologous recombination.Communications biology · 2026Article
- CTCF primes repressive chromatin for rapid BRCA1/BARD1 recruitment to drive homologous recombination repair of DNA double-strand breaks.Nucleic acids research · 2026Article
- The Landscape of BRCA1-Associated Post-Translational Modifications.Cell biology international · 2026Review
- Metabolic drivers of genome instability in cancer: mechanisms and therapeutic opportunities.Experimental hematology & oncology · 2026Review
- Chromatin Remodeling, DNA Double-Strand Break Repair, and Human Disease: How a Breakup Changes You.Biomolecules · 2026Review
- Saturation genome editing ofmedRxiv : the preprint server for health sciences · 2025Article
- Interplay and Dynamics of Chromatin Architecture and DNA Damage Response: An Overview.Cancers · 2025Review
- Identification of Estrogen-Responsive Proteins in Mouse Seminal Vesicles Through Mass Spectrometry-Based Proteomics.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Ribosomal S6 kinase (RSK) plays a critical role in DNA damage response via the phosphorylation of histone lysine demethylase KDM4B.Breast cancer research : BCR · 2024Article
- PHF8 facilitates transcription recovery following DNA double-strand break repair.Nucleic acids research · 2024Article
- HJURP is recruited to double-strand break sites and facilitates DNA repair by promoting chromatin reorganization.Oncogene · 2024Article
- Advances in DNA damage response inhibitors in colorectal cancer therapy.Acta biochimica et biophysica Sinica · 2024Review
- Dynamic de novo heterochromatin assembly and disassembly at replication forks ensures fork stability.Nature cell biology · 2023Article
- New perspectives on epigenetic modifications and PARP inhibitor resistance in HR-deficient cancers.Cancer drug resistance (Alhambra, Calif.) · 2023Article
- Alteration of Trop-2 expression in breast cancer cells by clinically used therapeutic agents and acquired tamoxifen resistance.Breast cancer (Tokyo, Japan) · 2022Article
- Transcriptional regulation and chromatin dynamics at DNA double-strand breaks.Experimental & molecular medicine · 2022Review
- DNA Damage Response Regulation by Histone Ubiquitination.International journal of molecular sciences · 2022Review
- Tumor Intrinsic PD-L1 Promotes DNA Repair in Distinct Cancers and Suppresses PARP Inhibitor-Induced Synthetic Lethality.Cancer research · 2022Article
- Roles for the methyltransferase SETD8 in DNA damage repair.Clinical epigenetics · 2022Review
- RIF1-ASF1-mediated high-order chromatin structure safeguards genome integrity.Nature communications · 2022Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Stable retention of BRCA1/BARD1 complexes at sites of DNA damage is required for the proper response to DNA double-strand breaks (DSB). Here, we demonstrate that the BRCT domain of BARD1 is crucial for its retention through interaction with HP1. In response to DNA damage, BARD1 interacts with Lys9-dimethylated histone H3 (H3K9me2) in an ATM-dependent but RNF168-independent manner. This interaction is mediated primarily by HP1γ. A conserved HP1-binding motif in the BARD1 BRCT domain directly interacted with the chromoshadow domain of HP1 in vitro. Mutations in this motif (or simultaneous depletion of all three HP1 isoforms) disrupted retention of BARD1, BRCA1, and CtIP at DSB sites and allowed ectopic accumulation of RIF1, an effector of nonhomologous end-joining, at damaged loci in S-phase. UNC0638, a small-molecule inhibitor of histone lysine methyltransferase (HKMT), abolished retention and cooperated with the PARP inhibitor olaparib to block cancer cell growth. Taken together, our findings show how BARD1 promotes retention of the BRCA1/BARD1 complex at damaged DNA sites and suggest the use of HKMT inhibitors to leverage the application of PARP inhibitors to treat breast cancer.
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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.