ArticlePLoS biology2006
A new description of cellular quiescence.
Article in PLoS biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 301 papers, 1 of them a synthesis that pooled it.
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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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Who cites it
301 citing papers in PubMed, 1 synthesis or guideline pooled it, 550 citations in OpenAlex.
- "Quiescence" in the resting zone of the growth plate: a systematic review.Stem cells (Dayton, Ohio) · 2026Pooled it
- Quiescence as an Active and Dynamic Regulator of Neural Stem Cells in Adult Olfactory Neurogenesis.The European journal of neuroscience · 2026Review
- Isolation of coelomocyte from sea urchin Echinometra mathaei: optimization of culture condition.In vitro cellular & developmental biology. Animal · 2026Article
- Spatial ecology of breast cancer reveals co-evolution of proliferative and dormant niches.Genome medicine · 2026Article
- Clinical Implications of Polyploid Giant Cancer Cells in Solid Tumors: Biology, Diagnosis, and Therapeutic Considerations.Cancers · 2026Review
- The dynamics of centromere assembly and disassembly during quiescence.The Journal of cell biology · 2026Article
- Mitochondria-ER contact sites (MERCS) in the cell cycle: molecular architecture and functional remodeling across cellular states.BMC biology · 2026Review
- G0 or no-G0: phosphatase control of quiescence and cell cycle entry.Biochemical Society transactions · 2026Review
- Article
- Multi-omics analysis reveals metabolic diversity underlying endothelial cell functions.Life science alliance · 2026Article
- Lineage-resolved lifetime modelling reveals potential quiescence and synchronization among MDA-MB-468 breast cancer cells.Frontiers in cell and developmental biology · 2026Article
- A multiscale model reveals how ERK/p38-regulated dormancy shapes tumor-immune dynamics and immunoediting outcomes.Frontiers in immunology · 2026Article
- Prolonged starvation deepens quiescence in Vasa2/Piwi1-expressing cells of a sea anemone.PLoS biology · 2025Article
- Dormant yet dangerous: the role of cell rest in perseverance.Future microbiology · 2025Review
- Investigations into the basal neural-like properties of dental pulp stem cells reveal they possess a functional type 2 muscarinic receptor which regulates quiescence.Stem cell research & therapy · 2025Article
- Ecological History Shapes Transcriptome Variation in QuiescentBiomolecules · 2025Article
- E2F1 induces a G0-G1 reentry transcriptional program without changing chromatin accessibility.bioRxiv : the preprint server for biology · 2025Article
- Stress granules promote quiescence by enhancing p21 levels and reducing phospho-Rb.RNA (New York, N.Y.) · 2025Article
- The dynamics of centromere assembly and disassembly during quiescence.bioRxiv : the preprint server for biology · 2025Article
- Guardians of silence: transcriptional networks in T cell quiescence.Experimental & molecular medicine · 2025Review
241 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular quiescence, defined as reversible growth/proliferation arrest, is thought to represent a homogenous state induced by diverse anti-mitogenic signals. We used transcriptional profiling to characterize human diploid fibroblasts that exited the cell cycle after exposure to three independent signals--mitogen withdrawal, contact inhibition, and loss of adhesion. We show here that each signal caused regulation of a unique set of genes known to be important for cessation of growth and division. Therefore, contrary to expectation, cells enter different quiescent states that are determined by the initiating signal. However, underlying this diversity we discovered a set of genes whose specific expression in non-dividing cells was signal-independent, and therefore representative of quiescence per se, rather than the signal that induced it. This fibroblast "quiescence program" contained genes that enforced the non-dividing state, and ensured the reversibility of the cell cycle arrest. We further demonstrate that one mechanism by which the reversibility of quiescence is insured is the suppression of terminal differentiation. Expression of the quiescence program was not simply a downstream consequence of exit from the cell cycle, because key parts, including those involved in suppressing differentiation, were not recapitulated during the cell cycle arrest caused by direct inhibition of cyclin-dependent kinases. These studies form a basis for understanding the normal biology of cellular quiescence.
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What OpenQuestion holds
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.