ArticlePLoS genetics2007
A transcriptional program mediating entry into cellular quiescence.
Article in PLoS genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 84 citations in OpenAlex.
- Comparison of volumetric dynamic optical coherence tomography with biological methods for evaluation of radiation effects in prostate tumor spheroids.Journal of biomedical optics · 2026Article
- Starvation activates ECM-remodeling gene transcription and putative enhancers in fibroblasts despite inducing quiescence.Cell reports · 2025Article
- Transcription factor networks in cellular quiescence.Nature cell biology · 2025Review
- Nutrient starvation activates ECM remodeling gene enhancers associated with inflammatory bowel disease risk in fibroblasts.bioRxiv : the preprint server for biology · 2024Article
- A cell cycle centric view of tumour dormancy.British journal of cancer · 2023Review
- Epigenetic instability caused by absence of CIZ1 drives transformation during quiescence cycles.BMC biology · 2023Article
- EMT/MET plasticity in cancer and Go-or-Grow decisions in quiescence: the two sides of the same coin?Molecular cancer · 2023Review
- Sorting-free metabolic profiling uncovers the vulnerability of fatty acid β-oxidation in in vitro quiescence models.Molecular systems biology · 2022Article
- Breast Cancer Metastasis: Mechanisms and Therapeutic Implications.International journal of molecular sciences · 2022Review
- Chromatin Dynamics During Entry to Quiescence and Compromised Functionality in Cancer Cells.Results and problems in cell differentiation · 2022Article
- Tamoxifen and oxidative stress: an overlooked connection.Discover oncology · 2021Review
- Control of endothelial quiescence by FOXO-regulated metabolites.Nature cell biology · 2021Article
- Resistance of Hypoxic Cells to Ionizing Radiation Is Mediated in Part via Hypoxia-Induced Quiescence.Cells · 2021Article
- The Adipokine Component in the Molecular Regulation of Cancer Cell Survival, Proliferation and Metastasis.Pathology oncology research : POR · 2021Review
- Antagonism between splicing and microprocessor complex dictates the serum-induced processing of lnc-RNA (New York, N.Y.) · 2020Article
- A post-transcriptional program of chemoresistance by AU-rich elements and TTP in quiescent leukemic cells.Genome biology · 2020Article
- Epigenetic silencing of SALL2 confers tamoxifen resistance in breast cancer.EMBO molecular medicine · 2019Article
- Stem Cell Quiescence: Dynamism, Restraint, and Cellular Idling.Cell stem cell · 2019Review
- Alternative polyadenylation factors link cell cycle to migration.Genome biology · 2018Article
- SALL2 represses cyclins D1 and E1 expression and restrains G1/S cell cycle transition and cancer-related phenotypes.Molecular oncology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The balance of quiescence and cell division is critical for tissue homeostasis and organismal health. Serum stimulation of fibroblasts is well studied as a classic model of entry into the cell division cycle, but the induction of cellular quiescence, such as by serum deprivation (SD), is much less understood. Here we show that SS and SD activate distinct early transcriptional responses genome-wide that converge on a late symmetric transcriptional program. Several serum deprivation early response genes (SDERGs), including the putative tumor suppressor genes SALL2 and MXI1, are required for cessation of DNA synthesis in response to SD and induction of additional SD genes. SDERGs are coordinately repressed in many types of human cancers compared to their normal counterparts, and repression of SDERGs predicts increased risk of cancer progression and death in human breast cancers. These results identify a gene expression program uniquely responsive to loss of growth factor signaling; members of SDERGs may constitute novel growth inhibitors that prevent cancer.
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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.