CDC25B
- Known as:
- CDC25B
- Catalog number:
- 000206A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CDC25B
Related genes to: CDC25B
- Gene:
- CDC25B NIH gene
- Name:
- cell division cycle 25B
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 1992-07-31
- Date modifiied:
- 2017-12-06
Related products to: CDC25B
Related articles to: CDC25B
- The global incidence of ulcerative colitis (UC) has significantly increased in rapidly industrializing nations, with numerous studies highlighting environmental exposures, particularly nitrogen dioxide (NO), as potential contributors to disease susceptibility. However, the clinical implications and molecular mechanisms linking NO exposure to UC susceptibility remain poorly understood. This study investigated the associations between NO and UC by integrating multi-omics data. We identified a CD8 T cell subpopulation with a distinct phenotype characterized by perforin production, which potentially exacerbated colonic inflammation related to NO exposure. To validate this hypothesis, we established mouse models exposed to NO, confirming increased CD8 T cell infiltration and elevated perforin secretion through immunofluorescent (IF) staining. Employing artificial intelligence techniques, we identified Cell Division Cycle 25B (CDC25B) as a gene of interest correlated with putative NO-related UC signatures. Finally, through molecular docking (MD) and molecular dynamics simulations (MDS), we identified ozanimod as one of several computationally nominated compounds associated with the CDC25B‑related network; however, none of these computational predictions were experimentally validated in the present study. Collectively, these findings suggest a correlative link between perforin or CD8 T cell-associated colonic inflammation and NO-associated UC susceptibility, and nominate CDC25B as a candidate gene for further investigation. - Source: PubMed
Publication date: 2026/08/30
Wang ZhijieChang XinFu TianXu DanMa YuanhongZhang HaoXia HubinZhang XiaofengHou Yingdong - - Source: PubMed
- Cancer originates from the uncontrolled proliferation of normal cells. Previous studies have demonstrated that CDC25B, a cell cycle-regulating phosphatase, is overexpressed in various tumors, including hepatocellular carcinoma, and its expression level may serve as a prognostic biomarker. The present study investigated the upstream miRNA regulators of CDC25B and demonstrated that their interactions can inhibit hepatocellular carcinoma progression. Here, stable hepatocellular carcinoma cell lines overexpressing or knocking down CDC25B were established using lentiviral vectors. The effects of CDC25B expression on the invasive phenotype of hepatocellular carcinoma cells were analyzed using plate cloning, scratch assays, and Transwell assays, and a subcutaneous tumor xenograft model in mice was established to evaluate the impact of CDC25B on tumor growth in vivo. Furthermore, dual-luciferase reporter assays were used to validate the targeted regulatory relationship between miR-200a-3p and CDC25B, while miR-200a-3p mimics and inhibitors were employed to elucidate the specific downstream mechanisms. We found that high expression of CDC25B significantly enhanced the epithelial-mesenchymal transition process, thereby accelerating the proliferation, invasion, and migration of hepatocellular carcinoma cells, whereas CDC25B knockdown exerted the opposite effects. In vivo tumorigenicity experiments in nude mice confirmed that overexpression of CDC25B promoted tumor growth. In addition, the dual-luciferase reporter assay confirmed that miR-200a-3p specifically targets and downregulates CDC25B expression, thereby inhibiting hepatocellular carcinoma progression. - Source: PubMed
Huang ZixiangYu Xi - Uveal melanoma (UM) is a challenging malignancy, in terms of diagnosis, risk stratification, and treatment associated with high morbidity and mortality rates. It has been demonstrated that E2F-related pathways play a significant role in the tumorigenesis and distant metastasis of UM. In this study, the E2F target-related genes were utilized to construct and validate a prognostic risk score for patients with UM. - Source: PubMed
Publication date: 2026/05/14
Al Sharie Ahmed HTashtoush Mais BDarweesh Reem FJadallah Rand KAl-Karaki Jawad MAl-Omari Samah OAleshawi Abdelwahab JAlqudah Asem AAlemam AmerAbu Serhan HashemElnahry Ayman GEl-Elimat TamamAl-Dwairi Rami - Palladium nanoparticles (Pd NPs), extensively used in automobile catalytic converters, are increasingly released into the environment and represent an emerging nanopollution concern for aquatic ecosystems. This study examined the chronic effects of environmentally relevant Pd NP exposure on the freshwater vertebrate model , integrating bioaccumulation analysis, oxidative stress profiling, histopathology, and bulk RNA-seq transcriptomics with computational cell-type inference analyses. Adult zebrafish were exposed for 42 days to low (0.4 ng/L) and high (22 ng/L) Pd NP concentrations. Inductively coupled plasma-mass spectrometry confirmed dose-dependent Pd bioaccumulation in whole-body tissues. Biochemical analyses indicated a disruption of gonadal redox homeostasis, characterized by altered activities of superoxide dismutase, catalase, glutathione S-transferase, glutathione reductase, and lipid peroxidation, indicating sustained oxidative stress. Histological examination of ovaries and testes demonstrated progressive structural damage, including follicular atresia, delayed oocyte maturation, and impaired spermatogenesis, highlighting reproductive vulnerability. Transcriptomic profiling showed concentration-dependent transcriptional changes under Pd NP exposure, including reduced expression of mitochondrial energy metabolism genes and increased expression of DNA repair, cell cycle regulation, steroid biosynthesis, and stress-response pathways. High-dose Pd exposure strongly increased the expression of cell cycle and stress-response genes, including ccnb1 (41 to 8296 TPM), cdc25b (41 to 1937 TPM), and tp53 (110 to 604 TPM), while mitochondrial energy metabolism genes were consistently suppressed. Notably, --, , and cell cycle signaling axes exhibited biphasic regulation, reflecting compensatory and maladaptive stress responses. This study identifies potential ecological and human health risks associated with palladium nanoparticle dispersal and emphasizes the need for safer catalyst design and stricter environmental management of platinum group nanoparticles. - Source: PubMed
Publication date: 2026/07/16
Pottanthara Ashokan AnilaEswaran MurugeshGovindhan ThiruppathiMathan Ramesh