ArticleProceedings of the National Academy of Sciences of the United States of America2013
Runx1 and p21 synergistically limit the extent of hair follicle stem cell quiescence in vivo.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed.
- Vascular endothelial cells as signaling niches for epithelial stem cells in the skin.Frontiers in cell and developmental biology · 2026Review
- Acetate drives ovarian cancer quiescence via ACSS2-mediated acetyl-CoA production.Molecular metabolism · 2024Article
- Ontogeny of Skin Stem Cells and Molecular Underpinnings.Current issues in molecular biology · 2024Review
- Acetate drives ovarian cancer quiescence via ACSS2-mediated acetyl-CoA production.bioRxiv : the preprint server for biology · 2024Article
- A negative feedback loop underlies the Warburg effect.NPJ systems biology and applications · 2024Article
- Recent progress in hair follicle stem cell markers and their regulatory roles.World journal of stem cells · 2024Review
- Deciphering the molecular mechanisms of stem cell dynamics in hair follicle regeneration.Experimental & molecular medicine · 2024Review
- RUN(X) out of blood: emerging RUNX1 functions beyond hematopoiesis and links to Down syndrome.Human genomics · 2023Review
- Article
- Regulation of adult stem cell quiescence and its functions in the maintenance of tissue integrity.Nature reviews. Molecular cell biology · 2023Review
- Single cell analysis of transcriptome and open chromatin reveals the dynamics of hair follicle stem cell aging.Frontiers in aging · 2023Article
- Review
- A RUNX-targeted gene switch-off approach modulates the BIRC5/PIF1-p21 pathway and reduces glioblastoma growth in mice.Communications biology · 2022Article
- Integrated analysis of lncRNAs and mRNAs by RNA-Seq in secondary hair follicle development and cycling (anagen, catagen and telogen) of Jiangnan cashmere goat (Capra hircus).BMC veterinary research · 2022Article
- Cell cycle-independent integration of stress signals by Xbp1 promotes Non-G1/G0 quiescence entry.The Journal of cell biology · 2022Article
- Cell cycle arrest determines adult neural stem cell ontogeny by an embryonic Notch-nonoscillatory Hey1 module.Nature communications · 2021Article
- Escape of hair follicle stem cells causes stem cell exhaustion during aging.Nature aging · 2021Article
- Stem cell-intrinsic mechanisms regulating adult hair follicle homeostasis.Experimental dermatology · 2021Review
- Stem cell quiescence: the challenging path to activation.Development (Cambridge, England) · 2021Review
- Histone H3 K4/9/27 Trimethylation Levels Affect Wound Healing and Stem Cell Dynamics in Adult Skin.Stem cell reports · 2020Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Mechanisms of tissue stem cell (SC) quiescence control are important for normal homeostasis and for preventing cancer. Cyclin-dependent kinase inhibitors (CDKis) are known inhibitors of cell cycle progression. We document CDKis expression in vivo during hair follicle stem cell (HFSC) homeostasis and find p21 (cyclin-dependent kinase inhibitor 1a, Cdkn1a), p57, and p15 up-regulated at quiescence onset. p21 appears important for HFSC timely onset of quiescence. Conversely, we find that Runx1 (runt related transcription factor 1), which is known for promoting HFSC proliferation, represses p21, p27, p57, and p15 transcription in HFSC in vivo. Intriguingly, in cell culture, tumors, and normal homeostasis, Runx1 and p21 interplay modulates proliferation in opposing directions under the different conditions. Unexpectedly, Runx1 and p21 synergistically limit the extent of HFSC quiescence in vivo, which antagonizes the role of p21 as a cell cycle inhibitor. Importantly, we find in cultured keratinocytes that Runx1 and p21 bind to the p15 promoter and synergistically repress p15 mRNA transcription, thereby restraining cell cycle arrest. This documents a surprising ability of a CDKi (p21) to act as a direct transcriptional repressor of another CDKi (p15). We unveil a robust in vivo mechanism that enforces quiescence of HFSCs, and a context-dependent role of a CDKi (p21) to limit quiescence of SCs, potentially by directly down-regulating mRNA levels of (an)other CDKi(s).
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Registered trials
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