ArticleProceedings of the National Academy of Sciences of the United States of America2011
Regulation of apoptosis by the circadian clock through NF-kappaB signaling.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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
65 citing papers in PubMed, 108 citations in OpenAlex.
- Investigation of the Effects of Saffron on Neuroprotection and Circadian Rhythm in anPharmaceuticals (Basel, Switzerland) · 2026Article
- Circadian clock control of breast cancer hallmarks: molecular mechanisms and therapeutic implications.Cancer metastasis reviews · 2026Review
- The interplay between circadian rhythm components and apoptosis in health and disease.Human cell · 2026Review
- Clock genes in pancreatic disease progression: from circadian regulation to dysfunction.Annals of medicine · 2025Review
- Circadian Clock Deregulation and Metabolic Reprogramming: A System Biology Approach to Tissue-Specific Redox Signaling and Disease Development.International journal of molecular sciences · 2025Review
- The roles of Cryptochrome-1: the circadian clock as a control point in cancer therapy.Journal of translational medicine · 2025Review
- The Effects of Circadian Rhythm on Lead-Induced Toxicity in the DBC1.2 Olfactory Dark Basal Cell Line.Cells · 2025Article
- Alterations in Circadian Rhythms, Sleep, and Physical Activity in COVID-19: Mechanisms, Interventions, and Lessons for the Future.Molecular neurobiology · 2024Review
- Telomere length and chronotype among women in the California Teachers Study (CTS).Chronobiology international · 2024Article
- The Biological Clock of Liver Metabolism in Metabolic Dysfunction-Associated Steatohepatitis Progression to Hepatocellular Carcinoma.Biomedicines · 2024Review
- Review
- Regulation of protein O-GlcNAcylation by circadian, metabolic, and cellular signals.The Journal of biological chemistry · 2024Review
- House dust mite and Th2 cytokine-mediated epithelial barrier dysfunction attenuation by KL001 in 16-HBE cells.Tissue barriers · 2024Article
- Integrated multi-omics analysis reveals the molecular interplay between circadian clocks and cancer pathogenesis.Scientific reports · 2023Article
- Circadian Rhythms and Astrocytes: The Good, the Bad, and the Ugly.Annual review of neuroscience · 2023Review
- Cryptochrome 2 acetylation attenuates its antiproliferative effect in breast cancer.Cell death & disease · 2023Article
- Chronic jetlag accelerates pancreatic neoplasia in conditionalChronobiology international · 2023Article
- Molecular regulations of circadian rhythm and implications for physiology and diseases.Signal transduction and targeted therapy · 2022Review
- It's About Time: The Circadian Network as Time-Keeper for Cognitive Functioning, Locomotor Activity and Mental Health.Frontiers in physiology · 2022Review
- NF-κB modifies the mammalian circadian clock through interaction with the core clock protein BMAL1.PLoS genetics · 2021Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In mice and humans the circadian rhythm of many biochemical reactions, physiology, and behavior is generated by a transcriptional-translation feedback loop (TTFL) made up of the so-called core clock genes/proteins. The circadian system interfaces with most signaling pathways including those involved in cell proliferation and inflammation. Cryptochrome (CRY) is a core clock protein that plays an essential role in the repressive arm of the TTFL. It was recently reported that mutation of CRY in p53-null mice delayed the onset of cancer. It was therefore suggested that CRY mutation may activate p53-independent apoptosis pathways, which eliminate premalignant and malignant cells and thus delay overt tumor formation. Here we show that CRY mutation sensitizes p53 mutant and oncogenically transformed cells to tumor necrosis factor α (TNFα)-initiated apoptosis by interfacing with the NF-κB signaling pathway through the GSK3β kinase and alleviating prosurvival NF-κB signaling. These findings provide a mechanistic foundation for the delayed onset of tumorigenesis in clock-disrupted p53 mutant mice and suggest unique therapeutic strategies for treating cancers associated with p53 mutation.
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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.