ZNF24 Antibody - N-terminal region (ARP33518_P050)
- Known as:
- ZNF24 Antibody - N-terminal region (ARP33518_P050)
- Catalog number:
- arp33518_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZNF24 Antibody - N-terminal region (ARP33518_P050)
Related genes to: ZNF24 Antibody - N-terminal region (ARP33518_P050)
- Gene:
- ZNF24 NIH gene
- Name:
- zinc finger protein 24
- Previous symbol:
- ZNF191
- Synonyms:
- ZSCAN3, Zfp191, KOX17
- Chromosome:
- 18q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-13
- Date modifiied:
- 2016-10-05
Related products to: ZNF24 Antibody - N-terminal region (ARP33518_P050)
Related articles to: ZNF24 Antibody - N-terminal region (ARP33518_P050)
- Mechanisms underlying breast cancer brain metastasis (BCBM) are still not well understood. Here, we identified that BCBM patient serum contained extracellular vesicles (EVs) with high levels of microRNAs (miRNAs)-107 and -425. Levels of miR-107 and miR-425 were elevated in brain metastases, and the elevation was associated with poor patient prognoses. Ectopic expression of miR-107 and miR-425 promoted mammospheres; however, the inhibition of miR-425, but not miR-107, suppressed breast cancer mammosphere formation. We further observed that EVs from miR-425-overexpressing breast cancer cells strongly activated astrocytes whereas their inhibitors abrogated the effect. Conditioned media from miR-425-activated astrocytes promoted mammospheres. To elucidate how miR-425 activates astrocytes, we found that, within astrocytes, miR-425 suppressed the expression of transcription factor ZNF24, which downregulated CCL8 cytokine expression/secretion, leading to the subsequent activation of astrocytes. Using a mouse study, we further determined the role of miR-425 in brain metastasis formation and observed that miR-425-overexpressing breast cancer cells exhibited significantly more aggressive growth in mouse brains compared to control cells. Immunohistochemistry and immunofluorescence analyses of mouse brain metastases revealed that miR-425-overexpressing tumors exhibited significantly increased activation, intratumoral accumulation, and proliferation of astrocytes, and a decrease in ZNF24 expression compared to control tumors. Together, our findings demonstrate, for the first time, that breast cancer EV-derived miR-425 promotes BCBM via activating astrocytes in the brain microenvironment through the novel EV-miR-425-ZNF24-CCL8 signaling axis. - Source: PubMed
Publication date: 2026/03/31
Wong Grace LKhan Munazza SManore SaraBindal ShivaniSingh RaviLo Hui-Wen - Chronic nonbacterial prostatitis (CNP) is a prevalent and refractory urogenital disorder whose immunopathogenic mechanisms remain incompletely understood. Given that redox imbalance is increasingly recognized as a critical driver of chronic inflammation, this study systematically investigated the role of epithelial redox stress in immune regulation during CNP and its underlying molecular mechanisms. By integrating plasma cytokine profiling, bulk and single-cell transcriptomic analyses, and experimental autoimmune prostatitis (EAP) models, we identified epithelial-derived macrophage migration inhibitory factor (MIF) as a central mediator driving chronic prostatic inflammation. Mechanistically, inflammatory injury induced excessive accumulation of reactive oxygen species (ROS) in epithelial cells, which in turn activated the redox-responsive transcription factor ZNF24 to bind the MIF promoter and promote its transcription. Epithelial cell-derived MIF acted in a paracrine manner on CD74-expressing macrophages. Engagement of CD74 by MIF stabilized PKM2 expression, enhanced macrophage glycolytic reprogramming, promoted PKM2 nuclear translocation, and activated NF-κB-dependent transcriptional programs, thereby driving M1 macrophage polarization and proinflammatory cytokine production. Pharmacological interventions targeting distinct key nodes of this signaling pathway-including inhibition of MIF (ISO-1), blockade of CD74 (neutralizing antibodies), stabilization of PKM2 tetramers (DASA-58), and suppression of NF-κB (JSH-23)-significantly attenuated prostatic inflammation, restored mitochondrial homeostasis, and alleviated pelvic pain in vitro or in vivo. Collectively, these findings define an epithelial ROS-ZNF24-MIF-macrophage CD74-PKM2-NF-κB signaling axis, through which coordinated enhancement of glycolytic reprogramming and inflammatory signaling promotes M1 macrophage polarization and drives the initiation and progression of CNP. Moreover, multiple redox-sensitive nodes within this pathway represent promising therapeutic targets for precision immunomodulation in CNP. - Source: PubMed
Publication date: 2026/01/20
Zhang FeiZhang AndongMeng TongLiu XianhongYang ChengLiang ChaozhaoZhang Meng - The imbalance of immune checkpoint molecules leads to immune escape of tumor cells. It has been established that KRAS mutation plays a key role in regulating PD-L1 expression of lung adenocarcinoma. However, the specific mechanism by which KRAS mutation regulates PD-L1 expression still needs further been clarified. - Source: PubMed
Publication date: 2025/09/02
Li LeileiFeng QiangJiang YaYang LilinFang HongXu WenmangWang YuanyuanPan XinyanYang Julun - To utilize the Traditional Chinese Medicine constitution (TCMC) as a complementary and alternative approach for early disease detection and treatment, with a focus on and deficiency constitutions, which serve as key references for disease prevention and management. - Source: PubMed
Xi LongZixuan W UYunfeng Y UJie LinQinghua Peng - Mechanisms underlying breast cancer brain metastasis (BCBM) are still not well understood. Here, we identified that BCBM patient serum contained extracellular vesicles (EVs) with high levels of microRNAs (miRNAs)-107 and -425. Levels of miR-107 and miR-425 were elevated in brain metastases, and the elevation was associated with poor patient prognoses. Ectopic expression of miR-107 and miR-425 promoted mammospheres; inhibition of miR-425, but not miR-107, suppressed breast cancer mammosphere formation. EVs from miR-425-overexpressing breast cancer cells strongly activated astrocytes whereas their inhibitors abrogated the effect. Conditioned media from miR-425-activated astrocytes promoted mammospheres. Within astrocytes, miR-425 suppressed expression of transcription factor ZNF24, which downregulated CCL8 cytokine expression/secretion, leading to subsequent activation of astrocytes. We further determined the role of miR-425 in brain metastasis formation and observed that miR-425-overexpressing breast cancer cells exhibited significantly more aggressive growth in mouse brains compared to control cells. Immunohistochemistry and immunofluorescence analysis of mouse brain metastases revealed that miR-425 tumors exhibited significantly increased activation, intratumoral accumulation, and proliferation of astrocytes, and a decrease in ZNF24 expression compared to control tumors. Together, our findings demonstrate that breast cancer EV-derived miR-425 promotes BCBM via activating astrocytes in the brain microenvironment through the novel EV-miR-425-ZNF24-CCL8 signaling axis. - Source: PubMed
Publication date: 2025/06/09
Wong Grace LKhan Munazza SManore SaraBindal ShivaniSingh RaviLo Hui-Wen