anti phospho cdc25c ser216 rabbit mab (Bioss)
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Bioss
anti phospho cdc25c ser216 rabbit mab
Anti Phospho Cdc25c Ser216 Rabbit Mab, supplied by Bioss, used in various techniques. Bioz Stars score: 93/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti phospho cdc25c ser216 rabbit mab/product/Bioss
Average 93 stars, based on 7 article reviews
Anti Phospho Cdc25c Ser216 Rabbit Mab, supplied by Bioss, used in various techniques. Bioz Stars score: 93/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti phospho cdc25c ser216 rabbit mab/product/Bioss
Average 93 stars, based on 7 article reviews
anti phospho cdc25c ser216 rabbit mab - by Bioz Stars,
2026-03
93/100 stars
Images
1) Product Images from "Multi-omics approach reveals TGF-β signaling-driven senescence in periodontium stem cells"
Article Title: Multi-omics approach reveals TGF-β signaling-driven senescence in periodontium stem cells
Journal: Journal of Advanced Research
doi: 10.1016/j.jare.2024.12.037
Figure Legend Snippet: TGF-β1-induced ROS accumulation leads to G2 arrest through ATM signaling. (A). RT-qPCR analysis of ATM signaling in TGF-β1 and/or its inhibitor-treated PDLSCs; (B). Western blot analysis of ATM signaling in TGF-β1 and/or its inhibitor-treated PDLSCs; (C). Western blot analysis of ATM signaling phosphorylated activation in the condition of ATM or CHK2 knockdown; (D). Western blot analysis of ATM signaling phosphorylated activation under N-acetyl-l-cysteine (NAC) treatment; (E). Western blot analysis of ATM signaling phosphorylated activation under decitabine treatment. Reagent doses and duration: TGF-β1 (10 ng/ml, 48 h), NAC (4 mM, 48 h), decitabine (10uM, 48 h). Predicted molecular weight: ATM 350 kDa, pATM 370 kDa, CDC25C&pCDC25C 60 kDa, CHK1&pCHK1 54 kDa, CHK2&pCHK2 62 kDa, β-Tubulin 55 kDa; GAPDH 37 kDa. Statistical significance: * p < 0.05, ** p < 0.01, *** p < 0.001, ns denotes not significant by one-way analysis of variance followed by the Tukey’s test. Error bars represent means ± SEM of at least three independent experiments.
Techniques Used: Quantitative RT-PCR, Western Blot, Activation Assay, Knockdown, Molecular Weight
Figure Legend Snippet: Proposed model for how TGF-β induces G2 arrest-related senescence in PDLSCs. TGF-β signaling induces irreversible G2 arrest in PDLSCs through the ATM signaling pathway in response to ROS accumulation and DNA damage. Specifically, TGF-β1-induced DNMTs expression, including DNMT1, DNMT3A, and DNMT3B, triggers the CpG sites hypermethylation in 5′UTR of PRKAG2 , encoding AMPKγ2, followed by its declined translation and ROS accumulation; meanwhile, NOX4 serves as another source of excessive ROS independent of DNA methylation. Overburdened ROS leads to DNA damage through the activation of the ATM-CHK-CDC25C axis. Of note, the phosphorylation of CDC25C in Ser216 impedes PDLSCs from entering into mitosis, disrupting the G2/M transition. Eventually, constant ROS stress and accumulated DNA damage impel the cell cycle to permanent stagnation, namely cellular senescence. Other well-established senescence-related proteins, including p16 and p21, may participate in maintaining G2 cell cycle arrest, awaiting further validation. Overall, our study demonstrates that TGF-β1 induces G2 arrest-related senescence in PDLSCs primarily due to epigenetic regulation, excessive ROS generation, and DNA damage.
Techniques Used: Expressing, DNA Methylation Assay, Activation Assay, Phospho-proteomics, Biomarker Discovery
