p21Waf1 is required for cellular senescence but not for cell cycle arrest induced by the HDAC inhibitor sodium butyrate
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Summary
The knockout of the p21Waf1 abolished most of the features of NaB-induced senescence, including irreversibility of cell cycle arrest, hypertrophy, additional focal adhesions and block of migration, gH2AX foci accumulation and SA-bGal staining.
- Type
- article
- Published
- 2010-10-01
- Cited by
- 88
- References
- 49
- Access
- Open access
- OpenAlex
- https://openalex.org/W1983215963
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:40119396
Keywords
Cell biology, Biology, Cell cycle checkpoint, Cell cycle, Sodium butyrate
References
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- Activation of the p21WAF1/CIP1 promoter independent of p53 by the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) through the Sp1 sites
- Chromatin structure and DNA double-strand break responses in cancer progression and therapy
- Cross‐talk between Ras and Rho signalling pathways in transformation favours proliferation and increased motility
- Aging and Immortality: Quasi-Programmed Senescence and Its Pharmacologic Inhibition
- Rho GTPases in cell biology
- The p65/RelA subunit of NF-kappaB interacts with actin-containing structures.
Cited by
- Answering the ultimate question “What is the Proximal Cause of Aging?”
- Rapamycin, proliferation and geroconversion to senescence
- An integrated approach for monitoring cell senescence.
- Ejercicio y envejecimiento: cambios transcripcionales y epigenéticos en un modelo murino de envejecimiento acelerado
- The Role of Nitric Oxide Dysregulation in Tumor Maintenance
- Histone deacetylase inhibitors cause TP53-dependent induction of p21/Waf1 in tumor cells with TP53 mutations
- NIAM, a novel activator of p53 and potential tumor suppressor
- The role of the MEK/ERK pathway in regulation of HDACI-induced senescence of transformed rat embryo fibroblasts
- Rhus coriaria induces senescence and autophagic cell death in breast cancer cells through a mechanism involving p38 and ERK1/2 activation
- Molecular damage in cancer: an argument for mTOR-driven aging
- IκB Kinase β (IKKβ) Inhibits p63 Isoform γ (TAp63γ) Transcriptional Activity*
- Mutations and Deregulation of Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Cascades Which Alter Therapy Response
- Mechanistic or mammalian target of rapamycin (mTOR) may determine robustness in young male mice at the cost of accelerated aging
- NCI's provocative questions on cancer: some answers to ignite discussion
- Novel functions of USP36 : regulation of histone 2B and the P53-MDM2 pathway through deubiquitination
- Butyrate suppresses murine mast cell proliferation and cytokine production through inhibiting histone deacetylase.
- Latest progress in tyrosine kinase inhibitors
- Downregulation of HMGA2 by the pan-deacetylase inhibitor panobinostat is dependent on hsa-let-7b expression in liver cancer cell lines.
- Rapamycin induces pluripotent genes associated with avoidance of replicative senescence
- p21Waf1 is required for complete oncogenic transformation of mouse embryo fibroblasts by E1Aad5 and c-Ha-ras oncogenes.
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