ArticleCell cycle (Georgetown, Tex.)2011
p27(Kip1) is required to maintain proliferative quiescence in the adult cochlea and pituitary.
Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 73 citations in OpenAlex.
- Acetate drives ovarian cancer quiescence via ACSS2-mediated acetyl-CoA production.Molecular metabolism · 2024Article
- Roles of supporting cells in the maintenance and regeneration of the damaged inner ear: A literature review.Journal of otology · 2024Review
- Acetate drives ovarian cancer quiescence via ACSS2-mediated acetyl-CoA production.bioRxiv : the preprint server for biology · 2024Article
- Endothelial Cell Flow-Mediated Quiescence Is Temporally Regulated and Utilizes the Cell Cycle Inhibitor p27.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Expression ofProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Endothelial cell flow-mediated quiescence is temporally regulated and utilizes the cell cycle inhibitor p27.bioRxiv : the preprint server for biology · 2024Article
- SoxC transcription factors shape the epigenetic landscape to establish competence for sensory differentiation in the mammalian organ of Corti.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- AAV-Net1 facilitates the trans-differentiation of supporting cells into hair cells in the murine cochlea.Cellular and molecular life sciences : CMLS · 2023Article
- Conserved Cdk inhibitors show unique structural responses to tyrosine phosphorylation.Biophysical journal · 2022Article
- Restoring the Cell Cycle and Proliferation Competence in Terminally Differentiated Skeletal Muscle Myotubes.Cells · 2021Review
- Review
- GATA3 maintains the quiescent state of cochlear supporting cells by regulating p27Scientific reports · 2021Article
- Cochlea cell-specific marker expression upon in vitro Hes1 knockdown.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021Article
- Serum deprivation initiates adaptation and survival to oxidative stress in prostate cancer cells.Scientific reports · 2020Article
- Requirement of PP2A-B56iScience · 2020Article
- Characterizing Adult Cochlear Supporting Cell Transcriptional Diversity Using Single-Cell RNA-Seq: Validation in the Adult Mouse and Translational Implications for the Adult Human Cochlea.Frontiers in molecular neuroscience · 2020Article
- Hair cell regeneration from inner ear progenitors in the mammalian cochlea.American journal of stem cells · 2020Review
- Renewed proliferation in adult mouse cochlea and regeneration of hair cells.Nature communications · 2019Article
- Multiple supporting cell subtypes are capable of spontaneous hair cell regeneration in the neonatal mouse cochlea.Development (Cambridge, England) · 2019Article
- The nuclear mitotic apparatus protein NuMA controls rDNA transcription and mediates the nucleolar stress response in a p53-independent manner.Nucleic acids research · 2017Article
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5 authors at 2 institutions in 2 countries.
Funding
Abstract
Cell cycle inhibitors, such as the cyclin-dependent kinase (Cdk) inhibitor proteins and retinoblastoma (Rb) family members, control exit from the cell cycle during the development of a variety of terminally differentiated tissues. It is unclear whether sustained expression of these proteins is required to prevent cell cycle re-entry in quiescent and terminally differentiated cells. The organ of Corti (cochlear sensory epithelium) and pars intermedia (intermediate lobe of the pituitary) are two tissues that share the characteristic of ongoing cell division in mice lacking either the p27(Kip1) Cdk inhibitor, Ink4 proteins, or Rb. Here, we use tamoxifen-inducible mouse models to delete p27(Kip1) in postnatal animals and show this is sufficient to induce proliferation in both the organ of Corti and pars intermedia. Thus, these tissues remain sensitive to the presence of p27(Kip1) even after their developmental exit from the cell cycle. The neonatal cochlea displayed heightened sensitivity to changes in p27(Kip1) expression, with a proliferative response higher than that of constitutive null mice. In adults, the proliferative response was reduced but was accompanied by increased cell survival. In contrast, re-establishment of normal p27(Kip1) expression in animals with established pituitary tumors, in an inducible "knock-on" model, led to cessation of pituitary tumor growth, indicating the cells had maintained their susceptibility to p27-mediated growth suppression. Although restoration of p27(Kip1) did not induce apoptosis, it did lead to resolution of pathological features and normalization of gene expression. Our data underscore the importance of p27(Kip1) expression in the maintenance of cellular quiescence and terminal differentiation.
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