ArticlePLoS genetics2018
Regulation of circadian clock transcriptional output by CLOCK:BMAL1.
Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.
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Who cites it
101 citing papers in PubMed, 1 synthesis or guideline pooled it, 178 citations in OpenAlex.
- Meta-analysis of Diurnal Transcriptomics in Mouse Liver Reveals Low Repeatability of Rhythm Analyses.Journal of biological rhythms · 2023Pooled it
- Role of the circadian rhythm in squamous cell carcinoma: From molecular mechanism to therapy (Review).Molecular medicine reports · 2026Review
- Stable clocks, rewired rhythms: circadian remodeling in skeletal muscle during aging, cachexia, and type 2 diabetes.Life metabolism · 2026Review
- Noncircadian BMAL1-YAP activity amplifies persistent inflammation in aged epidermis.Nature aging · 2026Article
- CLOCK/BMAL1 interactome uncovers homeodomain factors as tissue regulators.Nature cell biology · 2026Article
- Perturbation of the circadian rhythmic transcription contributes to radiotherapy-induced salivary gland hypofunction.Communications biology · 2026Article
- BMAL1 regulates circadian rhythms via phase separation-mediated transcriptional hub formation.Signal transduction and targeted therapy · 2026Article
- BMAL1 modulates glutamine supply to control haematopoietic stem and progenitor cell expansion.Development (Cambridge, England) · 2026Article
- Impact of acute blue light irradiation on the molecular clock and markers associated with photoaging in skin cell models.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Impact of E-Cigarette Use on Circadian Proteins and Cardiovascular Risk Markers.Journal of cardiovascular translational research · 2026Article
- Interplay between circadian and other transcription factors-Implications for cycling transcriptome reprogramming.FEBS letters · 2026Review
- ARNTL deregulation promotes ovarian cancer progression and metastasis by activating cancer-associated fibroblasts.Journal of ovarian research · 2026Article
- Broad Epigenetic Shifts in the Aging Drosophila Retina Contribute to Its Altered Diurnal Rhythmic Transcriptome.Aging cell · 2026Article
- Pharmacological Foundation and Novel Insights of Resveratrol in Cardiovascular System: A Review.Current cardiology reviews · 2026Review
- The Role of BMAL1 in Regulating Circadian Rhythms During Airway Remodeling in Asthma.Journal of immunology research · 2026Review
- Circadian clock and cancer.Military Medical Research · 2026Review
- Exploring the potential of miR-9a-5p in circadian rhythm and cognitive recovery following brain injury in neonatal rats.Functional & integrative genomics · 2025Article
- The sleep-wake history contributes to rhythmic BMAL1 chromatin binding in the cerebral cortex but not in the liver.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Circadian regulation of extracellular vesicle biogenesis, composition, and release.Npj biological timing and sleep · 2025Review
- PBAF/cBAF reorganization on H3.3 chromatin regulates BMAL1 activity in the absence of circadian negative feedback.Nature communications · 2025Article
41 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mammalian circadian clock relies on the transcription factor CLOCK:BMAL1 to coordinate the rhythmic expression of 15% of the transcriptome and control the daily regulation of biological functions. The recent characterization of CLOCK:BMAL1 cistrome revealed that although CLOCK:BMAL1 binds synchronously to all of its target genes, its transcriptional output is highly heterogeneous. By performing a meta-analysis of several independent genome-wide datasets, we found that the binding of other transcription factors at CLOCK:BMAL1 enhancers likely contribute to the heterogeneity of CLOCK:BMAL1 transcriptional output. While CLOCK:BMAL1 rhythmic DNA binding promotes rhythmic nucleosome removal, it is not sufficient to generate transcriptionally active enhancers as assessed by H3K27ac signal, RNA Polymerase II recruitment, and eRNA expression. Instead, the transcriptional activity of CLOCK:BMAL1 enhancers appears to rely on the activity of ubiquitously expressed transcription factors, and not tissue-specific transcription factors, recruited at nearby binding sites. The contribution of other transcription factors is exemplified by how fasting, which effects several transcription factors but not CLOCK:BMAL1, either decreases or increases the amplitude of many rhythmically expressed CLOCK:BMAL1 target genes. Together, our analysis suggests that CLOCK:BMAL1 promotes a transcriptionally permissive chromatin landscape that primes its target genes for transcription activation rather than directly activating transcription, and provides a new framework to explain how environmental or pathological conditions can reprogram the rhythmic expression of clock-controlled genes.
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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.