Cdc25b (phospho-Ser149) Antibody
- Known as:
- Cdc25b (phosphorilated-Ser149) Antibody
- Catalog number:
- abx000370
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- Cdc25b (phospho-Ser149) Antibody
Related genes to: Cdc25b (phospho-Ser149) Antibody
- 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 (phospho-Ser149) Antibody
Related articles to: Cdc25b (phospho-Ser149) Antibody
- 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 - Molecular and functional networks driving coordination between cell cycle and mRNA translation remain to be explored. Here, we use mass spectrometry-based proteomics to comprehensively investigate the interactome and phosphoproteome of the cell cycle regulator CDC25A. We identify actors of mRNA regulation, such as RNA-binding proteins and translation factors, as interacting partners of CDC25A. CDC25A overexpression increases global translation, whereas catalytic inactivation or pharmacological inhibition decreases protein synthesis. A Cyclin-Dependent Kinase (CDK) interaction-deficient mutant of CDC25A also enhances translation, indicating a CDK-independent role. Our results further reveal an interplay between CDC25A and CDC25B whereby downregulation of CDC25A leads to compensatory overexpression of CDC25B. The roles of CDC25A and CDC25B in mRNA translation are independent of their roles in the cell cycle, with CDC25A possibly regulating translation elongation and CDC25B rather involved in initiation. In acute myeloid leukemia cells, CDC25A depletion also inhibits translation, suggesting its potential relevance as a therapeutic target. We propose that CDC25 phosphatases might be signaling platforms coordinating cell cycle progression with protein synthesis. - Source: PubMed
Publication date: 2026/07/14
Shin SauyeunCargnello MariePinchedé LisaMedale Giamarchi ClaireVillette CléaGay AlexandreSalnot VirginieGautier Emilie-FleurDassi ErikMillevoi StefaniaCammas AnneManenti Stéphane - DNA methylation is an epigenetic modification that regulates gene expression in response to environmental exposures. We measured differential DNA methylation levels in blood before after general anesthesia and surgery in participants with and without postoperative delirium (POD) and postoperative neurocognitive disorder (PNCD). - Source: PubMed
Publication date: 2026/06/15
Hogan Kirk JBerger MilesKolstad Sydney PMadrid AndyHsia BethanyWright Mary CDevinney MichaelSmith Melody RAlisch Reid S - Early-life manganese (Mn) overexposure induces cognitive flexibility impairments by disrupting hippocampal neurogenesis and decreasing neural stem cells (NSCs) differentiation into neuroblasts. CDC25B is a key regulator required for both the cell cycle and NSCs differentiation. However, the association between energy metabolism conversion and Mn-related hippocampal neurogenesis malfunction, and whether this malfunction is caused by Cdc25b mRNA decay, remains unclear. This study utilized C57BL/6 mouse offspring and applied single-cell RNA sequencing to investigate the link between Mn-induced cognitive impairment and early-life neurogenesis disruption. The results showed that 1.1 mg/kg/day Mn exposure significantly impaired cognitive flexibility. This impairment was associated with disrupted NSCs differentiation into neuroblasts. Subsequently, we used primary NSCs to examine whether disrupted energy metabolism conversion affected METTL3-mediated Cdc25b mRNA decay. Aligned with this hypothesis, NSCs exposed to 50 μM Mn showed an unsuccessful transition from glycolysis to OXPHOS and an elevated METTL3-dependent Cdc25b mA modification, which led to reduced mRNA stability. In conclusion, Mn-associated inhibition of energy metabolism conversion in NSCs interrupts the CDC25B-regulated NSCs differentiation into neuroblasts in hippocampal neurogenesis. - Source: PubMed
Publication date: 2026/06/13
Cai Wei-JieLiu KuanLiu JieYao Tian-TianGuo Hui-MinXu BinMa Zhuo - Scleroderma citrinum (syn. Scleroderma aurantium and Scleroderma vulgare) is a mycorrhizal mushroom with known toxic effects but also holds potential for bioactive compound discovery. This study aimed to isolate and identify secondary metabolites from the fruiting bodies of S. citrinum and evaluate their potential antiviral and neuroprotective properties. - Source: PubMed
Publication date: 2026/05/25
Bolinget ElviraHsieh Cheng-YangSevilla Ureah TheaTsai Po-Wei