ArticleNucleic acids research2024
PHF8 facilitates transcription recovery following DNA double-strand break repair.
Article in Nucleic acids research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Molecular insights into DNA damage response plasticity in glioma stem cells.Communications biology · 2026Review
- DCAF13 Safeguards Hematopoietic Stem Cells via RRS1-Regulated Ribosome Biogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Phosphosite-centric regulatory network of ATAD2 and its involvement in transcriptional networks.Molecular genetics and genomics : MGG · 2026Article
- A novel dual histone mark reader ZCWPW2 regulates meiotic recombination through lactylation and transcriptional regulation in humans and mice.Nucleic acids research · 2026Article
- KDM7B-mediated demethylation of RNF113A regulates small cell lung cancer sensitivity to alkylation damage.bioRxiv : the preprint server for biology · 2026Article
- HER3 promotes triple-negative breast cancer progression by upregulating PHF8 via miR-34b-5p-dependent mechanism.Cell death & disease · 2025Article
- From silence to symphony: transcriptional repression and recovery in response to DNA damage.TranscriptionReview
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Transient halting of transcription activity on the damaged chromatin facilitates DNA double-strand break (DSB) repair. However, the molecular mechanisms that facilitate transcription recovery following DSB repair remain largely undefined. Notably, failure to restore gene expression in a timely manner can compromise transcriptome signatures and may impose deleterious impacts on cell identity and cell fate. Here, we report PHF8 as the major demethylase that reverses transcriptionally repressive epigenetic modification laid down by the DYRK1B-EHMT2 pathway. We found that PHF8 concentrates at laser-induced DNA damage tracks in a DYRK1B-dependent manner and promotes timely resolution of local H3K9me2 to facilitate the resumption of transcription. Moreover, PHF8 also assists in the recovery of ribosomal DNA (rDNA) transcription following the repair of nucleolar DSBs. Taken together, our findings uncover PHF8 as a key mediator that coordinates transcription activities during the recovery phase of DSB responses.
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Registered trials
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