ArticleNature communications2020
The bromodomain containing protein BRD-9 orchestrates RAD51-RAD54 complex formation and regulates homologous recombination-mediated repair.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 43 papers.
What it found
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Who cites it
43 citing papers in PubMed, 74 citations in OpenAlex.
- BRD proteins in human retroviral infection: emerging evidence from HIV-1 and future perspectives for HTLV-1.Molecular biology reports · 2026Review
- BAF chromatin remodeling complexes inhibit immediate-early and early, but not late, transcription of herpes simplex virus 1.bioRxiv : the preprint server for biology · 2026Article
- Epigenetic modifications in cancer drug resistance: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Review
- BRD9 at the crossroads of splicing, chromatin remodeling, and hematopoiesis.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2026Review
- USP29 and SMURF1 orchestrate FSP1-mediated ferroptosis suppression to facilitate chemoresistance in gastric cancer.Nature communications · 2025Article
- Key imidazolyl groups that induce phenylalanine flipping enhance the efficacy of oral BRD9 inhibitors for AML treatment.Acta pharmaceutica Sinica. B · 2025Article
- BRD9-p53-E2F1 circuit orchestrates cell growth and DNA damage repair in gastric cancer.Molecular cancer · 2025Article
- Chromatin remodeling and cancer: the critical influence of the SWI/SNF complex.Epigenetics & chromatin · 2025Review
- BRD4 regulates mActa pharmaceutica Sinica. B · 2025Article
- Targeting Bromodomain-Containing Protein 9 in Human Uterine Fibroid Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Chromatin remodeling complexes: architects influencing breast cancer progression.Frontiers in cell and developmental biology · 2025Review
- GLTSCR1 deficiency promotes colorectal cancer development through regulating non-homologous end joining.Oncogene · 2024Article
- Mammalian SWI/SNF complex activity regulates POU2F3 and constitutes a targetable dependency in small cell lung cancer.Cancer cell · 2024Article
- Syk-dependent homologous recombination activation promotes cancer resistance to DNA targeted therapy.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2024Article
- Frizzled class receptor 5 contributes to ovarian cancer chemoresistance through aldehyde dehydrogenase 1A1.Cell communication and signaling : CCS · 2024Article
- Targeting SWI/SNF Complexes in Cancer: Pharmacological Approaches and Implications.Epigenomes · 2024Review
- Overview of epigenetic degraders based on PROTAC, molecular glue, and hydrophobic tagging technologies.Acta pharmaceutica Sinica. B · 2024Review
- Bromodomain-Containing Protein 9 Regulates Signaling Pathways and Reprograms the Epigenome in Immortalized Human Uterine Fibroid Cells.International journal of molecular sciences · 2024Article
- Dimeric oxyberberine CT4-1 targets LINC02331 to induce cytotoxicity and inhibit chemoresistance via suppressing Wnt/β-catenin signaling in hepatocellular carcinoma.Archives of toxicology · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
17 authors at 5 institutions in 2 countries.
Funding
Abstract
Homologous recombination (HR) is important for error-free DNA double strand break repair and maintenance of genomic stability. However, upregulated HR is also used by cancer cells to promote therapeutic resistance. Therefore, inducing HR deficiency (HRD) is a viable strategy to sensitize HR proficient cancers to DNA targeted therapies in order to overcome therapeutic resistance. A bromodomain containing protein, BRD9, was previously reported to regulate chromatin remodeling and transcription. Here, we discover that following DNA damage, the bromodomain of BRD9 binds acetylated K515 on RAD54 and facilitates RAD54's interaction with RAD51, which is essential for HR. BRD9 is overexpressed in ovarian cancer and depleting BRD9 sensitizes cancer cells to olaparib and cisplatin. In addition, inhibitor of BRD9, I-BRD9, acts synergistically with olaparib in HR-proficient cancer cells. Overall, our results elucidate a role for BRD9 in HR and identify BRD9 as a potential therapeutic target to promote synthetic lethality and overcome chemoresistance.
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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.