The DOI matches its Crossref record; 29 of the 29 references it cites were found in a registry or an index.
Control of the Reversibility of Cellular Quiescence by the Transcriptional Repressor HES1
Open accessAbstract
The mechanisms by which quiescent cells, including adult stem cells, preserve their ability to resume proliferation after weeks or even years of cell cycle arrest are not known. We report that reversibility is not a passive property of nondividing cells, because enforced cell cycle arrest for a period as brief as 4 days initiates spontaneous, premature, and irreversible senescence. Increased expression of the gene encoding the basic helix-loop-helix protein HES1 was required for quiescence to be reversible, because HES1 prevented both premature senescence and inappropriate differentiation in quiescent fibroblasts. In some human tumors, the HES1 pathway was activated, which allowed these cells to evade differentiation and irreversible cell cycle arrest. We conclude that HES1 safeguards against irreversible cell cycle exit both during normal cellular quiescence and pathologically in the setting of tumorigenesis.
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“However, interruption of this pathway is no longer sufficient to rescue growth once the cells have progressed towards an established senescent phenotype (d'Adda di Fagagna et al, 2003; Sang et al, 2008).”
From Feedback between p21 and reactive oxygen production is necessary for cell senescence (2010) · cites this paper as Sang et al, 2008
Experimental — accuracy not yet measuredIn the citing paper
“The apparent discrepancy in our results may relate to cell type or species differences or the status of the helix-loop-helix protein HES1, which may play a crucial role in determining the reversibility of the quiescent state (Sang et al., 2008).”
From Dissecting the Unique Role of the Retinoblastoma Tumor Suppressor during Cellular Senescence (2010) · cites this paper as Sang et al., 2008
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Citations
Cites
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
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Cellular senescence: when bad things happen to good cells
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Inhibitors of mammalian G1 cyclin-dependent kinases.Preprint
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Self-citationRb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence
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Hematopoietic Stem Cell Quiescence Maintained by p21 cip1/waf1
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Notch Pathway Inhibition Depletes Stem-like Cells and Blocks Engraftment in Embryonal Brain Tumors
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Boulestreau, J., Maumus, M., Bertolino, G. M., Toupet, K., Jørgensen, C., & Noël, D. (2024) · Figshare · doi:10.6084/m9.figshare.25844441
An H4K20me3-CTCF switch at stable TAD boundaries enforces reversible cell state transitionsPreprint
Atai, K., Mitra, M., Bohn, E., Hu, R., Corvalan, A. Z., Jelínek, D., Voisin, L., Ambrus, A., Sarathy, K., Sparks, W. M., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.01.29.702647
Self-citationYakoubi, W. E. (2012) · theses.fr (ABES) · doi:10.70675/c7f12aa8zb750z4a9ez8b33za3e1f7ab1093
“La même équipe a pu montrer que Hes1 était nécessaire et suffisant à la prévention de la sénescence et de la différenciation des cellules quiescentes (Sang et al., 2008).”
BackgroundInfluentialIdentification et caractérisation de la fonction d’un réseau de gènes soumis à empreinte
Evano, B. (2012) · theses.fr (ABES) · doi:10.70675/145f92d8zdf33z4b39za037z390f530f7be0
Oscillatory Gene Expression During Cell Differentiation
Kageyama, R., & Isomura, A. (2026) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev-cellbio-111524-093438 · Cited by 1
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Baffoe, E. N., & Bouchnita, A. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1861769
Li, J., Zhang, N., Piao, M., Zhao, J., Wang, Y., Li, C., Li, S., Huang, Z., Li, Y., Xun, Z., et al. (2026) · Cancer and Metastasis Reviews · doi:10.1007/s10555-026-10392-5
Mihaliak, A. M. (2010) · eScholarship@UMassChan · doi:10.13028/j41x-ab26
“Quiescence helps preserve a stem cell‟s prolonged lifespan [51, 52], contributes to resistance to apoptosis [29, 53, 54], and prevents differentiation [55].”
Novel Regulation of the Cell Cycle During Cell Fate Decisions in the Central Nervous System
Lubanska, D. (2013) · Scholarship at UWindsor (University of Windsor)
Metadata
- Authors
- Sang, L., Coller, H. A., & Roberts, J. M.
- Affiliations
- Princeton University (US)
- Corresponding author
- Roberts, James M.
- Venue
- Science
- Published
- 2008-08-22
- Volume
- 321
- Issue
- 5892
- Pages
- 1095-1100
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC2721335
- OpenAlex
- W2018341322
- Cited by
- 313
- References
- 29
- Citations by year
- 2026: 9 · 2025: 12 · 2024: 12 · 2023: 10 · 2022: 7 · 2021: 10 · 2020: 12 · 2019: 16 · 2018: 14 · 2017: 16 · 2016: 13 · 2015: 17 · 2014: 25 · 2013: 23 · 2012: 33
- FWCI
- 18.74
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- National Cancer Institute (R01CA118043)
- National Institute of General Medical Sciences (P50GM071508)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- quiescent cells, Hes1, bHLH transcription factors, cell cycle arrest, premature senescence, fibroblasts, adult stem cells, carcinogenesis, cell cycle exit
- MeSH terms
- Transcription Factor HES-1, Cell Cycle, Cell Differentiation, Cell Line, Fibroblasts, Humans, Recombinant Fusion Proteins, Repressor Proteins, Rhabdomyosarcoma, Transduction, Genetic, Signal Transduction, Cellular Senescence, MyoD Protein, Homeodomain Proteins, Muscle Development, Cell Line, Tumor, Cell Proliferation, Cyclin-Dependent Kinase Inhibitor p21, Basic Helix-Loop-Helix Proteins, Receptors, Notch, Co-Repressor Proteins
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