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
- Invasive infections caused by have high mortality rates, even when treated with the first-line agent voriconazole. The global emergence of azole resistance further increases treatment failure, underscoring the urgent need for antifungals with novel mechanisms of action. The fungal cell cycle is essential for viability and represents an attractive but underexplored target. In , progression from G2 to M phase requires interaction between the phosphatase NimT and cyclin-dependent kinase NimX. Here, we characterize the role of this interaction and its inhibition by 2-fluoro-4-hydroxybenzonitrile (compound 1), a small molecule that targets the human Cdc25B-Cdk2 interface. Using mutagenesis, we show that NimT residues Arg438 and Arg442 are critical for NimT-NimX binding and confirm they are essential for viability. A co-immunoprecipitation assay demonstrates that compound 1 disrupts the interaction, while live-cell imaging shows that this inhibition arrests cell cycle progression. Our findings provide mechanistic insight into fungal mitosis and highlight cell cycle regulators as promising antifungal drug targets.IMPORTANCEInvasive aspergillosis has high mortality and limited treatment options, threatened by rising drug resistance. Targeting the fungal cell cycle represents an unexplored strategy for antifungal drug development. The dynamic interaction between NimT and NimX is critical to the fungal duplication cycle. Here, we show evidence that, unlike in , relocation of NimT from the nucleus to the cytoplasm mid-interphase is the switching event that causes activation of NimX and allows the cell cycle to progress. We also show that disruption of the NimT-NimX interaction can be achieved using a reversible small-molecule inhibitor that arrests the fungal duplication cycle, highlighting mitotic regulators as promising antifungal drug targets. - Source: PubMed
Publication date: 2026/04/29
Storer I S RThornton B PHackett A STabernero LBromley M J - Obeticholic acid (OCA), a potent agonist of the bile salt-activated nuclear receptor farnesoid X receptor (FXR), accelerates liver hypertrophy after portal vein embolization (PVE), but the mechanisms underlying this effect are incompletely understood. In a rabbit model of PVE, New Zealand White rabbits received OCA (10 mg/kg/day) or vehicle by oral gavage before and after embolization. We quantified systemic and hepatic bile salt pools, profiled FXR-regulated genes in ileum and liver, and related these parameters to volumetric and histological indices of regeneration. OCA shifted bile salt composition towards a more hydrophobic profile and improved homeostasis, with earlier normalization of serum total bile salts, reduced bile salt content in the non-embolized (hypertrophic) lobe, and lower circulating levels of the hepatotoxic bile salt lithocholic acid. Serum lithocholic acid strongly and inversely correlated with both caudal liver volume gain and hepatocyte proliferation. In the hypertrophic lobe, OCA markedly suppressed expression of CYP7A1, reduced circulating levels of the bile salt synthesis marker 7-alpha-hydroxy-4-cholesten-3-one, and increased expression of the basolateral bile salt exporter SLC51A/B, consistent with reduced bile salt synthesis and enhanced sinusoidal efflux. OCA also induced the mitotic entry regulator CDC25B. RNA sequencing identified ileal and hepatic signaling candidates, including C1q subunits, bone morphogenetic protein 3 (BMP3), and Indian hedgehog (IHH), which correlated with liver growth. These data indicate that FXR agonism by OCA promotes PVE-induced liver regeneration by improving bile salt homeostasis and modulating gut-liver growth signaling, supporting further evaluation of FXR agonists to enhance future liver remnant hypertrophy before major hepatectomy. - Source: PubMed
Publication date: 2026/04/18
Chang XinweiOlthof Pim BJin HanChau StevenSoons Zitavan Eijk Hansvan Golen Rowanvan Gulik Thomas MJansen Peter LDamink Steven W M OldeHeger MichalSchaap Frank G - The molecular mechanisms by which the human CDC25B activates the CDK1/cyclin B complex in the cell cycle, as well as how it can be inhibited by synthetic inhibitors at the atomic level, are still under investigation. Valuable insights have been gained from the molecular structure here-described, which captures for the first time the interaction between the C-terminal domain of the inactive mutant CDC25B C473S (CDC25B-S) and the commonly used synthetic substrate 3-O-methylfluorescein phosphate (3-OMFP). Crystallographic studies reveal that 3-OMFP engages multiple residues within the active site and the adjacent "swimming pool" of CDC25B-S, establishing specific interactions and prompting local adjustments in this region. These structural features explain the increased resistance to thermal denaturation of CDC25B-S observed through circular dichroism measurements upon substrate binding. The structural changes induced by 3-OMFP lead to a conformation comparable to that of CDC25A bound to its substrate, the CDK2/cyclin A complex. These findings qualify 3-OMFP as a promising starting model for the rational design of selective competitive inhibitors of CDC25B having reduced off-target effects. - Source: PubMed
Troisi RomualdoRullo RosarioNapolitano ValeriaPopowicz Grzegorz MDe Vendittis EmmanueleSica Filomena - Pediatric gliomas, comprising both low-grade (LGGs) and high-grade gliomas (HGGs), exhibit significant molecular and clinical heterogeneity. While LGGs generally have a favorable prognosis, HGGs are associated with poor long-term survival despite aggressive treatment. Advances in molecular profiling have enabled targeted therapies, but treatment resistance and tumor heterogeneity remain major challenges. The integration of artificial intelligence (AI) and transcriptomic data holds promise for refining prognostic models and guiding personalized treatment strategies, yet its application in pediatric gliomas remains underexplored. - Source: PubMed
Publication date: 2026/03/09
Li GanglongPei FuyuWang Weizhen - The greater amberjack () is a globally important aquaculture fish species belonging to the family Carangidae. However, current research on the ovarian development and regulation of the greater amberjack is limited, particularly with regard to early ovarian development in artificially bred individuals. Therefore, this study aims to analyze the ovarian transcriptomes at the primary growth stage in one-year-old fish at the chromatin nucleolar stage and two-year-old fish at the perinucleolar stage to suggest how early ovarian development takes place in artificially bred greater amberjacks. To do this, the study constructed ovarian mRNA expression profiles of different stages of artificially bred fish and identified differentially expressed genes (DEGs), Gene Ontology terms, and Kyoto Encyclopedia of Genes and Genomes pathways important for various physiological processes. A functional analysis revealed that the DEGs closely related to ovarian development were involved in cell growth and death (e.g., , , , , , and ), the TGF-beta signaling pathway (e.g., , , , , , and ), steroid hormone biosynthesis (e.g., , , and ), and the endocrine system (e.g., , , , and ). These findings suggest that ovarian development is the result of the coordinated regulation of various genes responsible for various functions. This study provides a theoretical basis for exploring the underlying molecular mechanisms of early ovarian development in artificially bred greater amberjacks. - Source: PubMed
Publication date: 2026/02/25
Deng QiuxiaHuang YangRu XiaoyingLin HaoyiYou XinxinHao RuijuanLi HangHu QinZhang DongyingZhao YanfeiWu JinhuiLi GuangliZhu Chunhua