ArticleNucleic acids research2011
Bromodomain protein 7 interacts with PRMT5 and PRC2, and is involved in transcriptional repression of their target genes.
Article in Nucleic acids research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.
- Clinicopathological and Prognostic Significance of PRMT5 in Cancers: A System Review and Meta-Analysis.Cancer control : journal of the Moffitt Cancer CenterPooled it
- MTAP Deficiency as a Metabolic Vulnerability in Cancer: Implications for Synthetic Lethal Therapy.Cancer science · 2026Review
- PRMT5 deficiency in myeloid cells reprograms macrophages to enhance antitumor immunity and synergizes with anti-PD-L1 therapy.Journal for immunotherapy of cancer · 2025Article
- BRD7 facilitates ferroptosis via modulating clusterin promoter hypermethylation and suppressing AMPK signaling in diabetes-induced testicular damage.Molecular medicine (Cambridge, Mass.) · 2024Article
- GlPRMT5 inhibits GlPP2C1 via symmetric dimethylation and regulates the biosynthesis of secondary metabolites in Ganoderma lucidum.Communications biology · 2024Article
- BRD7 suppresses tumor chemosensitivity to CHK1 inhibitors by inhibiting USP1-mediated deubiquitination of CHK1.Cell death discovery · 2023Article
- Epigenetic Regulation of HIV-1 Sense and Antisense Transcription in Response to Latency-Reversing Agents.Non-coding RNA · 2023Article
- Discovery and Biological Characterization of PRMT5:MEP50 Protein-Protein Interaction Inhibitors.Journal of medicinal chemistry · 2022Article
- Design, Synthesis and Biological Evaluation of Novel and Potent Protein Arginine Methyltransferases 5 Inhibitors for Cancer Therapy.Molecules (Basel, Switzerland) · 2022Article
- PRMT5: a putative oncogene and therapeutic target in prostate cancer.Cancer gene therapy · 2022Review
- BRD7 Stabilizes P53 via Dephosphorylation of MDM2 to Inhibit Tumor Growth in Breast Cancer Harboring Wild-type P53.Journal of Cancer · 2022Article
- PRMT5 promotes colorectal cancer growth by interaction with MCM7.Journal of cellular and molecular medicine · 2021Article
- Genome-wide chromatin occupancy of BRDT and gene expression analysis suggest transcriptional partners and specific epigenetic landscapes that regulate gene expression during spermatogenesis.Molecular reproduction and development · 2021Article
- PRMT5 Is Involved in Spermatogonial Stem Cells Maintenance by RegulatingFrontiers in cell and developmental biology · 2021Article
- PRMT5 functionally associates with EZH2 to promote colorectal cancer progression through epigenetically repressing CDKN2B expression.Theranostics · 2021Article
- BRD7 inhibits tumor progression by positively regulating the p53 pathway in hepatocellular carcinoma.Journal of Cancer · 2021Article
- ATM-Dependent Recruitment of BRD7 is required for Transcriptional Repression and DNA Repair at DNA Breaks Flanking Transcriptional Active Regions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- PRMT5 promotes DNA repair through methylation of 53BP1 and is regulated by Src-mediated phosphorylation.Communications biology · 2020Article
- PRMT5 function and targeting in cancer.Cell stress · 2020Review
- Islet-specific Prmt5 excision leads to reduced insulin expression and glucose intolerance in mice.The Journal of endocrinology · 2020Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Histone modification regulates gene expression, and one major regulatory step in this process is the ability of proteins that recognize epigenetic marks to recruit enzymes required to specify transcriptional outcome. Here we show that BRD7 is a component of hSWI-SNF complexes that interacts with PRMT5 and PRC2. Recruitment studies revealed that BRD7 co-localizes with PRMT5 and PRC2 on 'suppressor of tumorigenecity 7' (ST7) and retinoblastoma-like protein 2 (RBL2) promoters in patient-derived B cell lines, and that its association with these target genes correlates with hypermethylation of H3R8, H4R3 and H3K27. Furthermore, inhibition of BRD7 expression reduces PRMT5 and PRC2 recruitment to ST7 and RBL2 promoters; however, only ST7 becomes transcriptionally derepressed. Evaluation of the PRMT5- and PRC2-induced epigenetic marks revealed that while H3(Me(2))R8, H4(Me(2))R3 and H3(Me(3))K27 marks are erased from the ST7 promoter, demethylation of RBL2 promoter histones is incomplete. We also show that the arginine demethylase (RDM) JMJD6, which can erase PRMT5-induced H4R3 methylation, and the H3K27-lysine-specific demethylases, KDM6A/UTX and KDM6B/JMJD3, are differentially recruited to ST7 and RBL2. These findings highlight the role played by BRD7 in PRMT5- and PRC2-induced transcriptional silencing, and indicate that recruitment of specific RDMs and KDMs is required for efficient transcriptional derepression.
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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.