ArticleProceedings of the National Academy of Sciences of the United States of America2020
Screen identifies DYRK1B network as mediator of transcription repression on damaged chromatin.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- Expanding Synthetic Lethality in DNA Damage Response-Defective Cancers Through Stress Phenotype-Guided Kinase Targeting.International journal of molecular sciences · 2026Review
- Phosphoproteomics identifies the DYRK1B protein kinase as a regulator of processing bodies.Journal of cell science · 2026Article
- Oxidative stress triggers RNAPII arrest through PARylation and DNA damage.Nature communications · 2026Article
- Stabilization of AFF1 by PARylation ensures transcriptional restart after DNA damage.Nature chemical biology · 2026Article
- DYRK1B Inhibition by AZ191 Sensitizes High-Grade Serous Ovarian Cancer to Niraparib Through Promoting Apoptosis and Ferroptosis.Biomedicines · 2026Article
- Targeting DYRKs in Cardiovascular Diseases: From Biological Mechanisms to Therapeutic Translation.International journal of molecular sciences · 2026Review
- The protein kinase DYRK1B is a p53 target gene and functions as a negative feedback regulator of the transcription factor RFX7.Cell death & disease · 2026Article
- The EHMT2-MBLAC2 axis suppresses ribosomal DNA transcription in response to nucleolar DNA damage.Cell death & disease · 2026Article
- Nucleoporins cooperate with Polycomb silencers to promote transcriptional repression and repair at DNA double-strand breaks.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- DYRK1B phosphorylates FOXO1 to promote hepatic gluconeogenesis.Nucleic acids research · 2025Article
- hnRNPA2B1 deacetylation by SIRT6 restrains local transcription and safeguards genome stability.Cell death and differentiation · 2025Article
- Autophosphorylation of the Tousled-like kinases TLK1 and TLK2 regulates recruitment to damaged chromatin via PCNA interaction.Nucleic acids research · 2025Article
- Review
- Traffic light at DSB-transit regulation between gene transcription and DNA repair.FEBS letters · 2025Review
- Rapid effects of valproic acid on the fetal brain transcriptome: implications for brain development and autism.Translational psychiatry · 2024Article
- Elevated expression levels of the protein kinase DYRK1B induce mesenchymal features in A549 lung cancer cells.BMC cancer · 2024Article
- Differential regulation of expression of the protein kinases DYRK1A and DYRK1B in cancer cells.Scientific reports · 2024Article
- PHF8 facilitates transcription recovery following DNA double-strand break repair.Nucleic acids research · 2024Article
- Hepatic Dyrk1b impairs systemic glucose homeostasis by modulating Wbp2 expression in a kinase activity-dependent manner.Heliyon · 2024Article
- Nuclear F-actin assembly on damaged chromatin is regulated by DYRK1A and Spir1 phosphorylation.Nucleic acids research · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
DNA double-strand breaks (DSBs) trigger transient pausing of nearby transcription, an emerging ATM-dependent response that suppresses chromosomal instability. We screened a chemical library designed to target the human kinome for new activities that mediate gene silencing on DSB-flanking chromatin, and have uncovered the DYRK1B kinase as an early respondent to DNA damage. We showed that DYRK1B is swiftly and transiently recruited to laser-microirradiated sites, and that genetic inactivation of DYRK1B or its kinase activity attenuated DSB-induced gene silencing and led to compromised DNA repair. Notably, global transcription shutdown alleviated DNA repair defects associated with DYRK1B loss, suggesting that DYRK1B is strictly required for DSB repair on active chromatin. We also found that DYRK1B mediates transcription silencing in part via phosphorylating and enforcing DSB accumulation of the histone methyltransferase EHMT2. Together, our findings unveil the DYRK1B signaling network as a key branch of mammalian DNA damage response circuitries, and establish the DYRK1B-EHMT2 axis as an effector that coordinates DSB repair on transcribed chromatin.
Indexed as
Identifiers
What OpenQuestion holds
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.