ReviewFrontiers in physiology2020
A Systems Biology Approach Identifies Hidden Regulatory Connections Between the Circadian and Cell-Cycle Checkpoints.
Review in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Chronotherapy in Oncology: Aligning Cancer Treatment with Biological Time.Journal of personalized medicine · 2026Review
- Clock genes in pancreatic disease progression: from circadian regulation to dysfunction.Annals of medicine · 2025Review
- Circadian regulation of extracellular vesicle biogenesis, composition, and release.Npj biological timing and sleep · 2025Review
- The Common Hallmarks and Interconnected Pathways of Aging, Circadian Rhythms, and Cancer: Implications for Therapeutic Strategies.Research (Washington, D.C.) · 2025Review
- The circadian clock as a potential biomarker and therapeutic target in pancreatic cancer.Molecular and cellular biochemistry · 2024Review
- Biological clock regulation by theFrontiers in cell and developmental biology · 2024Review
- Chronobiology of Parkinson's disease: Past, present and future.The European journal of neuroscience · 2023Review
- Multi-synchronization and other patterns of multi-rhythmicity in oscillatory biological systems.Interface focus · 2022Review
- Circadian clock synchrony and chronotherapy opportunities in cancer treatment.Seminars in cell & developmental biology · 2022Review
- A transcriptomics-guided drug target discovery strategy identifies receptor ligands for lung regeneration.Science advances · 2022Article
- Mathematical analysis of robustness of oscillations in models of the mammalian circadian clock.PLoS computational biology · 2022Article
- Systematic modeling-driven experiments identify distinct molecular clockworks underlying hierarchically organized pacemaker neurons.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- A detailed map of coupled circadian clock and cell cycle with qualitative dynamics validation.BMC bioinformatics · 2021Article
- Thyroid Cancer and Circadian Clock Disruption.Cancers · 2020Review
- Circadian Genes as Therapeutic Targets in Pancreatic Cancer.Frontiers in endocrinology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Circadian rhythms form a self-sustaining, endogenous, time-keeping system that allows organisms to anticipate daily environmental changes. The core of the clock network consists of interlocking transcriptional-translational feedback loops that ensures that metabolic, behavioral, and physiological processes run on a 24 h timescale. The hierarchical nature of the clock manifests itself in multiple points of control on the daily cell division cycle, which relies on synthesis, degradation, and post-translational modification for progression. This relationship is particularly important for understanding the role of clock components in sensing stress conditions and triggering checkpoint signals that stop cell cycle progression. A case in point is the interplay among the circadian factor PERIOD2 (PER2), the tumor suppressor p53, and the oncogenic mouse double minute-2 homolog protein (MDM2), which is the p53's negative regulator. Under unstressed conditions, PER2 and p53 form a stable complex in the cytosol and, along with MDM2, a trimeric complex in the nucleus. Association of PER2 to the C-terminus end of p53 prevents MDM2-mediated ubiquitylation and degradation of p53 as well as p53's transcriptional activation. Remarkably, when not bound to p53, PER2 acts as substrate for the E3-ligase activity of MDM2; thus, PER2 is degraded in a phosphorylation-independent fashion. Unexpectedly, the phase relationship between PER2 and p53 are opposite; however, a systematic modeling approach, inferred from the oscillatory time course data of PER2 and p53, aided in identifying additional regulatory scenarios that explained,
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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.