ArticleNucleic acids research2021
A DYRK1B-dependent pathway suppresses rDNA transcription in response to DNA damage.
Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 22 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
- RNA Helicase DDX21 Controls CD4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 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
- Nucleolar Organization in Response to Transcriptional Stress.Cancer science · 2025Review
- DYRK1B phosphorylates FOXO1 to promote hepatic gluconeogenesis.Nucleic acids research · 2025Article
- Review
- 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
- Calmodulin Triggers Activity-Dependent rRNA Biogenesis via Interaction with DDX21.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Drug targets regulate systemic metabolism and provide new horizons to treat nonalcoholic steatohepatitis.Metabolism open · 2024Review
- Insights from the protein interaction Universe of the multifunctional "Goldilocks" kinase DYRK1A.Frontiers in cell and developmental biology · 2023Review
- A high-throughput assay for directly monitoring nucleolar rRNA biogenesis.Open biology · 2022Article
- Moderate Dose Irradiation Induces DNA Damage and Impairments of Barrier and Host Defense in Nasal Epithelial Cells in vitro.Journal of inflammation research · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA double-strand breaks (DSBs) at ribosomal gene loci trigger inhibition of ribosomal DNA (rDNA) transcription and extensive nucleolar reorganization, including the formation of nucleolar caps where rDNA DSBs engage with canonical DSB signaling and repair factors. While these nucleolar responses underlie maintenance of rDNA stability, the molecular components that drive each of these events remain to be defined. Here we report that full suppression of rRNA synthesis requires the DYRK1B kinase, a nucleolar DSB response that can be uncoupled from ATM-mediated DSB signaling events at the nucleolar periphery. Indeed, by targeting DSBs onto rDNA arrays, we uncovered that chemical inhibition or genetic inactivation of DYRK1B led to sustained nucleolar transcription. Not only does DYRK1B exhibit robust nucleolar accumulation following laser micro-irradiation across cell nuclei, we further showed that DYRK1B is required for rDNA DSB repair and rDNA copy number maintenance, and that DYRK1B-inactivated cells are hypersensitised to DSBs induced at the rDNA arrays. Together, our findings not only identify DYRK1B as a key signaling intermediate that coordinates DSB repair and rDNA transcriptional activities, but also support the idea of specialised DSB responses that operate within the nucleolus to preserve rDNA integrity.
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.