ReviewCurrent genetics2017
A common strategy for initiating the transition from proliferation to quiescence.
Review in Current genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mitochondrial Dysfunction and Induction of Apoptosis in Hepatocellular Carcinoma and Cholangiocarcinoma Cell Lines by Thymoquinone.International journal of molecular sciences · 2022Pooled it
- Article
- Deep learning-driven imaging of cell division and cell growth across an entire eukaryotic life cycle.Molecular biology of the cell · 2025Article
- Dual regulation of the levels and function of Start transcriptional repressors drives G1 arrest in response to cell wall stress.Cell communication and signaling : CCS · 2025Article
- Quiescent cells maintain active degradation-mediated protein quality control requiring proteasome, autophagy, and nucleus-vacuole junctions.The Journal of biological chemistry · 2025Article
- The longevity and reversibility of quiescence inCell cycle (Georgetown, Tex.) · 2023Article
- E2F4DN Transgenic Mice: A Tool for the Evaluation of E2F4 as a Therapeutic Target in Neuropathology and Brain Aging.International journal of molecular sciences · 2022Review
- Cell cycle-independent integration of stress signals by Xbp1 promotes Non-G1/G0 quiescence entry.The Journal of cell biology · 2022Article
- Diverse geroprotectors differently affect a mechanism linking cellular aging to cellular quiescence in budding yeast.Oncotarget · 2022Article
- E2F4-Based Gene Therapy Mitigates the Phenotype of the Alzheimer's Disease Mouse Model 5xFAD.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Tumor suppressor stars in yeast G1/S transition.Current genetics · 2021Review
- Replication-independent instability of Friedreich's ataxia GAA repeats during chronological aging.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Chromatin structure restricts origin utilization when quiescent cells re-enter the cell cycle.Nucleic acids research · 2021Article
- Cellular quiescence in budding yeast.Yeast (Chichester, England) · 2021Review
- High-Throughput Flow Cytometry Combined with Genetic Analysis Brings New Insights into the Understanding of Chromatin Regulation of Cellular Quiescence.International journal of molecular sciences · 2020Article
- Mechanisms that Link Chronological Aging to Cellular Quiescence in Budding Yeast.International journal of molecular sciences · 2020Review
- Genetic interaction profiles of regulatory kinases differ between environmental conditions and cellular states.Molecular systems biology · 2020Article
- Gcn5 and Rpd3 have a limited role in the regulation of cell cycle transcripts during the G1 and S phases in Saccharomyces cerevisiae.Scientific reports · 2019Article
- On the duration of the microbial lag phase.Current genetics · 2019Review
- Quiescence, an individual journey.Current genetics · 2019Review
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.
Funding
Abstract
Development, tissue renewal and long term survival of multi-cellular organisms is dependent upon the persistence of stem cells that are quiescent, but retain the capacity to re-enter the cell cycle to self-renew, or to produce progeny that can differentiate and re-populate the tissue. Deregulated release of these cells from the quiescent state, or preventing them from entering quiescence, results in uncontrolled proliferation and cancer. Conversely, loss of quiescent cells, or their failure to re-enter cell division, disrupts organ development and prevents tissue regeneration and repair. Understanding the quiescent state and how cells control the transitions in and out of this state is of fundamental importance. Investigations into the mechanics of G1 arrest during the transition to quiescence continue to identify striking parallels between the strategies used by yeast and mammals to regulate this transition. When cells commit to a stable but reversible arrest, the G1/S genes responsible for promoting S phase must be inhibited. This process, from yeast to humans, involves the formation of quiescence-specific complexes on their promoters. In higher cells, these so-called DREAM complexes of E2F4/DP/RBL/MuvB recruit the highly conserved histone deacetylase HDAC1, which leads to local histone deacetylation and repression of S phase-promoting transcripts. Quiescent yeast cells also show pervasive histone deacetylation by the HDAC1 counterpart Rpd3. In addition, these cells contain quiescence-specific regulators of G1/S genes: Msa1 and Msa2, which can be considered components of the yeast equivalent of the DREAM complex. Despite a lack of physical similarities, the goals and the strategies used to achieve a reversible transition to quiescence are highly conserved. This motivates a detailed study of this process in the simple model organism: budding yeast.
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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.