ArticleThe Journal of biological chemistry2009
Phosphorylated extracellular signal-regulated protein kinases 1 and 2 phosphorylate Sp1 on serine 59 and regulate cellular senescence via transcription of p21Sdi1/Cip1/Waf1.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 34 citations in OpenAlex.
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- TRIM59 expression is regulated by Sp1 and Nrf1 in LPS-activated macrophages through JNK signaling pathway.Cellular signalling · 2020Article
- An Effective Model of the Retinoic Acid Induced HL-60 Differentiation Program.Scientific reports · 2017Article
- Survive or thrive: tradeoff strategy for cellular senescence.Experimental & molecular medicine · 2017Review
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- Regulations of Reversal of Senescence by PKC Isozymes in Response to 12-O-Tetradecanoylphorbol-13-Acetate via Nuclear Translocation of pErk1/2.Molecules and cells · 2016Article
- Sgk1 enhances RANBP1 transcript levels and decreases taxol sensitivity in RKO colon carcinoma cells.Oncogene · 2013Article
- H2O2 accumulation mediates differentiation capacity alteration, but not proliferative decline, in senescent human fetal mesenchymal stem cells.Antioxidants & redox signaling · 2013Article
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- Transforming growth factor-β-inducible early response gene 1 is a novel substrate for atypical protein kinase Cs.Cellular and molecular life sciences : CMLS · 2011Article
- Conversion of Helicobacter pylori CagA from senescence inducer to oncogenic driver through polarity-dependent regulation of p21.The Journal of experimental medicine · 2010Article
- Minireview: modulation of hormone receptor signaling by dietary anticancer indoles.Molecular endocrinology (Baltimore, Md.) · 2009Review
- Alterations in microRNA expression in stress-induced cellular senescence.Mechanisms of ageing and developmentArticle
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2 authors at 1 institution in 1 country.
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Abstract
Expression of p21(Sdi1) downstream of p53 is essential for induction of cellular senescence, although cancer cell senescence can also occur in the p53 null condition. We report herein that senescence-associated phosphorylated extracellular signal-regulated protein kinases 1 and 2 (SA-pErk1/2) enhanced p21(Sdi1) transcription by phosphorylating Sp1 on Ser(59) downstream of protein kinase C (PKC) alpha. Reactive oxygen species (ROS), which was increased in cellular senescence, significantly activated both PKCalpha and PKCbetaI. However, PKCalpha, but not PKCbetaI, regulated ROS generation and cell proliferation in senescent cells along with activation of cdk2, proven by siRNAs. PKCalpha-siRNA also reduced SA-pErk1/2 expression in old human diploid fibroblast cells, accompanied with changes of senescence phenotypes to young cell-like. Regulation of SA-pErk1/2 was also confirmed by using catalytically active PKCalpha and its DN-mutant construct. These findings strongly suggest a new pathway to regulate senescence phenotypes by ROS via Sp1 phosphorylation between PKCalpha and SA-pErk1/2: employing GST-Sp1 mutants and MEK inhibitor analyses, we found that SA-pErk1/2 regulated Sp1 phosphorylation on the Ser(59) residue in vivo, but not threonine, in cellular senescence, which regulated transcription of p21(Sdi1) expression. In summary, PKCalpha, which was activated in senescent cells by ROS strongly activated Erk1/2, and the SA-pErk1/2 in turn phosphorylated Sp1 on Ser(59). Sp1-enhanced transcription of p21(Sdi1) resulted in regulation of cellular senescence in primary human diploid fibroblast cells.
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