Recombinant Human Cell Division Cycle 25A CDC25A
- Known as:
- Recombinant Human Cell Division Cycle 25A CDC25A
- Catalog number:
- enz-091
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- Recombinant Human Cell Division Cycle 25A CDC25A
Related genes to: Recombinant Human Cell Division Cycle 25A CDC25A
- Gene:
- CDC25A NIH gene
- Name:
- cell division cycle 25A
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1992-07-31
- Date modifiied:
- 2017-12-06
Related products to: Recombinant Human Cell Division Cycle 25A CDC25A
Related articles to: Recombinant Human Cell Division Cycle 25A CDC25A
- Cell division cycle 25A (CDC25A) is a key regulator of cell cycle progression, DNA replication and apoptosis in cancer cells. This study employed multiple well-characterised breast cancer cohorts to evaluate the prognostic significance of CDC25A and to characterise the molecular association linked to its expression in early-stage breast cancer. - Source: PubMed
Publication date: 2026/04/01
Kariri Yousif AAlsaleem Mansour AAlshamsan BaderAlgharras AbdulazizKariri Taher ARakha Emad A - Endometriosis is a common gynecological disorder affecting women of reproductive age, often leading to chronic pain, reduced quality of life, and infertility. It is characterized by ectopic endometrial growth within a hypoxic peritoneal environment. Autophagy, a cellular recycling pathway, is elevated in ectopic lesions. However, how hypoxia regulates autophagy to drive lesion development remains unclear. We found that inhibition of autophagy with chloroquine reduced stromal cell growth under hypoxia. The microRNA miR-21-5p, previously shown to be elevated by hypoxia in ectopic lesions, was examined and found to target cell division cycle 25A (CDC25A). Overexpression of miR-21-5p suppressed CDC25A. Under hypoxia, yes-associated protein 1 (YAP1) nuclear accumulation increased miR-21-5p, which in turn further reduced CDC25A expression. Silencing CDC25A enhanced autophagic flux, whereas pharmacologic inhibition of YAP1 with verteporfin restored CDC25A and p62 in mouse lesions and reduced lesion size. Collectively, these findings demonstrate that hypoxia activates YAP1-driven miR-21-5p, which represses CDC25A to promote autophagy and sustain lesion survival, highlighting the miR-21-5p/CDC25A axis as a potential therapeutic target. - Source: PubMed
Publication date: 2026/03/30
Hou Huan-TzuTsai Ya-ChuanLin Shih-ChiehPan Po-HungWu Meng-HsingTsai Shaw-Jenq - - Source: PubMed
Publication date: 2025/11/17
Wang MeiZhan PengSong Yuning - 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 - This study aims to systematically investigate the molecular mechanisms through which parabens may contribute to head and neck squamous cell carcinoma (HNSCC) carcinogenesis using integrated network toxicology and molecular docking. - Source: PubMed
Publication date: 2026/03/23
Zhao LeiYang JianwangLiu TaoCao HuanYu MiaomiaoWang Baoshan