CDC25A (phospho-Ser76) Antibody
- Known as:
- CDC25A (phosphorilated-Ser76) Antibody
- Catalog number:
- abx000369
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- CDC25A (phospho-Ser76) Antibody
Related genes to: CDC25A (phospho-Ser76) Antibody
- 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: CDC25A (phospho-Ser76) Antibody
Related articles to: CDC25A (phospho-Ser76) Antibody
- Cullin-RING ligase 4 (CRL4) complexes achieve substrate specificity through DDB1-CUL4-associated factors (DCAFs), yet how individual DCAFs engage the adaptor protein DDB1 remains incompletely understood. Here, we report the cryo-electron microscopy structure of DCAF8 in complex with DDB1 (2.53 Å) and define the molecular determinants underlying CRL4 assembly and cell cycle progression. Our structure reveals that DCAF8 associates with DDB1 primarily through an N-terminal helix-loop-helix (HLH) motif that inserts into a conserved pocket formed by the BPA and BPC domains of DDB1. Disruption of this interface impairs complex assembly, attenuates CDC25A ubiquitination, and results in cell cycle defects. In contrast, residues within the conserved double DxR box of DCAF8 are positioned away from the DDB1 interface and are dispensable for adaptor binding. Together, these findings define a DCAF8-specific recruitment mechanism within CRL4 ubiquitin ligase assemblies. - Source: PubMed
Publication date: 2026/06/02
Shen MiaomiaoZhang HangChen MinYang JiaqiYuchi ZhiguangZhang HuaweiLiu Liren - Esophageal squamous cell carcinoma (ESCC) is aggressive with poor prognosis, frequently driven by chemotherapy resistance. Kinesin family member 18B (KIF18B) is implicated in tumor progression, but its role in ESCC chemoresistance remains unclear. To investigate KIF18B's clinical relevance and mechanistic contribution to oxaliplatin resistance in ESCC, KIF18B expression was analyzed in TCGA data, ESCC cell lines/tissues (qPCR, Western blot, IHC), and correlated with survival (Kaplan-Meier). Results showed that, KIF18B was significantly elevated in ESCC and correlated with shorter overall/progression-free survival. Knockdown reversed oxaliplatin resistance, reducing IC50 from 8.5 µM to 3 µM, restoring apoptosis, and inducing G2/M arrest. Silencing suppressed the ATR/CHK1 pathway (reduced p-ATR, p-CHK1, WEE1, CDC25A) and increased γH2AX foci. Co-IP confirmed KIF18B-ATR interaction, suggesting stabilization of DNA damage signaling. In vivo, KIF18B knockdown synergized with oxaliplatin, achieving > 80% tumor suppression and reduced Ki-67/p-ATR/p-CHK1 levels. In conclusion, KIF18B is a prognostic biomarker and therapeutic target in ESCC. Its inhibition overcomes oxaliplatin resistance by disrupting KIF18B-ATR interaction and ATR/CHK1-mediated DNA repair. Combining KIF18B targeting with chemotherapy or ATR inhibitors represents a promising strategy for refractory ESCC. - Source: PubMed
Publication date: 2026/05/27
Liu WeiWang QianruTan XiaoCao ChunyuTian Bole - 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
Hou Huan-TzuTsai Ya-ChuanLin Shih-ChiehPan Po-HungWu Meng-HsingTsai Shaw-Jenq - - Source: PubMed
Publication date: 2025/11/17
Wang MeiZhan PengSong Yuning