CDC25C (Phospho-Ser198) Antibody
- Known as:
- CDC25C (Phospho-Ser198) Antibody
- Catalog number:
- 11790
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- CDC25C (Phospho-Ser198) Antibody
Related genes to: CDC25C (Phospho-Ser198) Antibody
- Gene:
- CDC25C NIH gene
- Name:
- cell division cycle 25C
- Previous symbol:
- CDC25
- Synonyms:
- PPP1R60
- Chromosome:
- 5q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-06
- Date modifiied:
- 2017-12-06
Related products to: CDC25C (Phospho-Ser198) Antibody
Related articles to: CDC25C (Phospho-Ser198) Antibody
- Sinonasal inverted papilloma is a locally aggressive epithelial lesion with a relatively high recurrence rate, yet the molecular basis of its proliferative behaviour remains incompletely understood. This study investigated the clinical relevance of secreted phosphoprotein 1 in sinonasal inverted papilloma and its association with epithelial cell proliferation and related signalling pathways. - Source: PubMed
Publication date: 2026/04/28
Tang WenruiWang LinYan XudongZhang JishengYu LonggangChen HanZheng ChungeDong ZihuiZheng QianyouHan LinJiang Yan - Polyethylene terephthalate (PET), one of the most widely used synthetic polymers globally, has emerged as a potential environmental risk factor for human health. However, the molecular mechanisms linking PET exposure to hepatocellular carcinoma (HCC) remain poorly understood. - Source: PubMed
Publication date: 2026/04/22
Chen PengLiu XinYuan DongmeiZheng LanDu YuminGong DacaiWei XingWang DanXu GeGe Bin - Subsequently to the publication of the above article, a concerned reader drew to the Editor's attention that the β‑actin bands featured in Fig. 1A were also apparently included in the 'Ctrl' experiments for the phospho‑P53 protein bands in Fig. 1B. In addition, a specific pair of P53 bands in Fig. 1B had also apparently been re‑used as phospho‑CDC25C bands in Fig. 6A, suggesting that these figures may have potentially undergone inappropriate editing. After having evaluated these data independently in the Editorial Office, the concerns of the reader were shown to have been well‑founded. Therefore, in view of the uncertainties regarding the assembly of some of the western blot data in Figs. 1 and 6, the Editor of has decided that this paper should be retracted from the Journal on account of uncertainties with the presentation of the abovementioned data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply.The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 35: 2707‑2714, 2016; DOI: 10.3892/or.2016.4674]. - Source: PubMed
Publication date: 2026/04/30
Zhang RuopengZhu LiZhang LirongXu AnliLi ZhengweiXu YijuanHe PeiWu MaoqingWei FengxiangWang Chenhong - Benzo(a)pyrene (BaP), an environmental carcinogen, contributes to colon cancer pathogenesis through incompletely elucidated mechanisms. This study integrated network toxicology and multi-omics analyses to decipher BaP-associated molecular signatures and clinical relevance in colon cancer. Using TCGA-COAD data, 113 differentially expressed BaP-related targets were identified via CTD and Super-PRED databases. PPI networks, functional enrichment, and Cox/Lasso regression revealed key pathways (xenobiotic metabolism, p53 signaling, cell cycle) and six prognostic genes (CLK2, CRYAB, RPS6KA1, DPP7, CDC25C, GAST). A BaP-related risk model stratified patients into distinct survival groups. A nomogram accurately predicted 1-, 3-, and 5-year overall survival. High-risk scores correlated with advanced tumor stage, metastasis, and immunosuppressive microenvironments. Molecular docking demonstrated strong BaP binding to CLK2 and CRYAB. External validation (GSE39582, TNMplot) confirmed tumor-specific gene expression patterns. These findings delineate BaP-driven networks connecting xenobiotic stress, immune dysregulation, and tumor progression. The risk model provides a prognostic biomarker for personalized management and therapeutic targeting in colon cancer. - Source: PubMed
Publication date: 2026/04/22
Yang XueyingYang ZhendongSui Bowen - The splicing kinase family contributes significantly to tumor progression. As a member of this family, PRPF4B has been directly implicated in oncogenic processes. However, little is known about the precise role and underlying mechanisms of PRPF4B in hepatocellular carcinoma (HCC). In this study, we found that the expression of PRPF4B was upregulated and associated with a poor prognosis in HCC patients. PRPF4B knockdown significantly suppressed HCC cell proliferation, migration, and invasion while concurrently inducing apoptosis. Knockdown of PRPF4B induced DNA damage via reactive oxygen species (ROS) accumulation, leading to cell cycle arrest at the G2/M phase. This arrest was associated with increased phosphorylation of CDC2, elevated γ-H2AX levels, and downregulation of CDC25C and cyclin B1. In addition, we found that expression of PRPF4B was upregulated in sorafenib no-responders (NR) compared with sorafenib responders (R). PRPF4B knockdown sensitizes HCC cells to sorafenib treatment. Mechanistically, we demonstrated that knockdown of PRPF4B inhibited HCC proliferation through NF-κB pathway. Furthermore, PRPF4B interacts with TIA1. Knockdown of PRPF4B promotes the expression of a specific TIA1 splice variant, leading to altered mRNA splicing that inhibits NF-κB activity. Our findings reveal that PRPF4B interacts with TIA1 and modulates its splicing. Knockdown of PRPF4B triggers ROS-dependent DNA damage, cell cycle arrest, and suppression of HCC proliferation, while enhancing sorafenib sensitivity via inhibition of the NF-κB pathway. Therefore, PPRF4B may be a potential therapeutic target for HCC treatment and sorafenib sensitization. - Source: PubMed
Publication date: 2026/04/01
Zhang CanxueHuang ZhihongSu YutingLiu YuqiZhang ChiGe ChaoTian WeiYang YueTian Hua