ArticleCell cycle (Georgetown, Tex.)2013
S6K in geroconversion.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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
26 citing papers in PubMed, 27 citations in OpenAlex.
- Senotherapy for chronic lung disease.Pharmacological reviews · 2025Review
- Article
- S6 kinase 1 at the central node of cell size and ageing.Frontiers in cell and developmental biology · 2022Review
- Ribosomal Protein S6: A Potential Therapeutic Target against Cancer?International journal of molecular sciences · 2021Review
- Anti-aging: senolytics or gerostatics (unconventional view).Oncotarget · 2021Review
- The goal of geroscience is life extension.Oncotarget · 2021Article
- Does rapamycin slow down time?Oncotarget · 2018Article
- Rapamycin, proliferation and geroconversion to senescence.Cell cycle (Georgetown, Tex.) · 2018Article
- From rapalogs to anti-aging formula.Oncotarget · 2017Review
- ZRF1 is a novel S6 kinase substrate that drives the senescence programme.The EMBO journal · 2017Article
- Gerosuppression by pan-mTOR inhibitors.Aging · 2016Article
- Six plant extracts delay yeast chronological aging through different signaling pathways.Oncotarget · 2016Article
- Evidence that hematopoietic stem cell function is preserved during aging in long-lived S6K1 mutant mice.Oncotarget · 2016Article
- Article
- Article
- Article
- Rejuvenating immunity: "anti-aging drug today" eight years later.Oncotarget · 2015Article
- MDM2 turnover and expression of ATRX determine the choice between quiescence and senescence in response to CDK4 inhibition.Oncotarget · 2015Article
- Tumor promoter-induced cellular senescence: cell cycle arrest followed by geroconversion.Oncotarget · 2014Article
- Koschei the immortal and anti-aging drugs.Cell death & disease · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Markers of cellular senescence depend in part on the MTOR (mechanistic target of rapamycin) pathway. MTOR participates in geroconversion, a conversion from reversible cell cycle arrest to irreversible senescence. Recently we demonstrated that hyper-induction of cyclin D1 during geroconversion was mostly dependent on MEK, whereas rapamycin only partially inhibited cyclin D1 accumulation. Here we show that, while not affecting cyclin D1, siRNA for p70S6K partially prevented loss of RP (replicative/regenerative potential) during p21-induced cell cycle arrest. Similarly, an inhibitor of p70 S6 kinase (PF-4708671) partially inhibited phosphorylation of S6 and preserved RP, while only marginally prevented cyclin D1 induction. Thus S6K and MEK play different roles in geroconversion.
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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.