ArticleOncogene2023
BMAL1 collaborates with CLOCK to directly promote DNA double-strand break repair and tumor chemoresistance.
Article in Oncogene, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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.
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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.
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Who cites it
30 citing papers in PubMed, 33 citations in OpenAlex.
- BMAL1 silencing as a promising chemosensitizing strategy for triple-negative breast cancer.Acta pharmacologica Sinica · 2026Article
- Time matters: circadian genetics and the molecular logic of human health and disease.Nature reviews. Genetics · 2026Review
- Deciphering the circadian signature in acute myeloid leukemia: NPAS2 downregulation as a master predictive feature.Blood research · 2026Article
- The circadian architecture of tumor immunity: mechanistic insights and treatment strategies.Biomarker research · 2026Review
- Can Disruption of Circadian Rhythms Be Linked to Radiation-Induced Acute Myeloid Leukaemia?Cancers · 2026Review
- DNA-PK-mediated CRTC2 phosphorylation promotes NHEJ and suppresses antitumor immunity via relocation to repair complexes.Nature communications · 2026Article
- BMAL2 is a druggable target for ovarian clear cell carcinoma (OCCC).EMBO molecular medicine · 2026Article
- BMAL1 Drives Cisplatin Resistance in Non-Small Cell Lung Cancer Via Lactate-MRP1 Signaling Pathway.Thoracic cancer · 2026Article
- The case for space as a model of accelerated aging.Nature aging · 2026Review
- Post-Translational Modifications in Animal Circadian Clocks.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- The interplay between circadian rhythm components and apoptosis in health and disease.Human cell · 2026Review
- SULT1A1 at a differentiation branch point regulates osteosarcoma cell proliferation and melatonin-mediated anti-tumor activity.Frontiers in oncology · 2026Article
- TCM-Driven Circadian Modulation in Cancer: Engineering Spatiotemporal Drug Delivery for Precision Oncology.International journal of nanomedicine · 2026Review
- Circadian clock and cancer.Military Medical Research · 2026Review
- Circadian regulation of homologous recombination by cryptochrome1-mediated dampening of DNA end resection.Nature communications · 2025Article
- Circadian rhythm in gastrointestinal cancer: clinical applications and future perspectives.Annals of medicine · 2025Review
- Circadian genesJournal of Zhejiang University. Science. B · 2025Review
- Role of circadian CLOCK signaling in cellular senescence.Biogerontology · 2025Review
- The diverse roles of the circadian clock in cancer.Nature cancer · 2025Review
- Decoding Multifaceted Roles of Sleep-Related Genes as Molecular Bridges in Chronic Disease Pathogenesis.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence indicates a correlation between circadian dysfunction and genomic instability. However, whether the circadian machinery directly regulates DNA damage repair, especially in double-strand breaks (DSBs), remains poorly understood. Here, we report that in response to DSBs, BMAL1 is activated by ATM-mediated phosphorylation at S183. Phosphorylated BMAL1 is then localized to DNA damage sites, where it facilitates acetylase CLOCK to load in the chromatin, regulating the acetylation of histone H4 (H4Ac) at DSB sites. In this way, the BMAL1-CLOCK-H4Ac axis promotes the DNA end-resection to generate single-stranded DNA (ssDNA) and the subsequent homologous recombination (HR). BMAL1 deficient cells display defective HR, accumulation of unrepaired DSBs and genome instability. Accordingly, depletion of BMAL1 significantly enhances the sensitivity of adrenocortical carcinoma (ACC) to DNA damage-based therapy in vitro and in vivo. These findings uncover non-canonical function of BMAL1 and CLOCK in HR-mediated DSB repair, which may have an implication in cancer therapeutics.
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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.