Ncoa4 antibody - N-terminal region (ARP37744_P050)
- Known as:
- Ncoa4 (anti-) - N-terminal region (ARP37744_P050)
- Catalog number:
- arp37744_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Ncoa4 antibody - N-terminal region (ARP37744_P050)
Related genes to: Ncoa4 antibody - N-terminal region (ARP37744_P050)
- Gene:
- NCOA4 NIH gene
- Name:
- nuclear receptor coactivator 4
- Previous symbol:
- -
- Synonyms:
- ARA70, RFG, ELE1, PTC3, DKFZp762E1112
- Chromosome:
- 10q11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-17
- Date modifiied:
- 2016-10-05
Related products to: Ncoa4 antibody - N-terminal region (ARP37744_P050)
Related articles to: Ncoa4 antibody - N-terminal region (ARP37744_P050)
- As an independent risk factor for atherosclerosis (AS), hyperhomocysteinemia (HHcy) exerts its pathogenic effects primarily through the induction of macrophage ferroptosis. As a selective autophagic process mediated by nuclear receptor coactivator 4 (NCOA4), ferritinophagy directly influences ferroptosis via its regulation of cellular iron balance. However, whether homocysteine (Hcy) regulates macrophage ferroptosis through ferritinophagy remains unclear. - Source: PubMed
Publication date: 2026/08/12
Yang YuZhang WeiyaHuang Dandan - Sarcopenia is an age-related pathological syndrome characterized by progressive and generalized loss of skeletal muscle mass and function, with muscle atrophy representing its cardinal pathological hallmark. Ferroptosis, an iron-dependent regulated cell death, has been implicated in the pathogenesis of muscle atrophy; however, the precise role of iron dysregulation in sarcopenia remains incompletely understood. In the present study, we identified ferroptosis in D-galactose (D-gal)-induced senescent myoblasts, as evidenced by elevated intracellular iron levels and lipid peroxidation, increased malondialdehyde (MDA) content, and upregulated expression of prostaglandin endoperoxide synthase 2 (PTGS2), 4-hydroxynonenal (4-HNE), and long-chain acyl-CoA synthetase 4 (ACSL4), accompanied by diminished glutathione peroxidase 4 (GPX4), SLC7A11 (xCT), and glutathione (GSH) levels, as well as pronounced mitochondrial damage. Notably, treatment with the iron chelator deferoxamine (DFO) significantly attenuated senescence-associated ferroptosis. Moreover, D-gal-induced senescence in myoblasts was accompanied by reduced ferritin expression and elevated nuclear receptor coactivator 4 (NCOA4) levels, both of which were reversed by autophagy inhibition with 3-methyladenine (3-MA) or NCOA4 knockdown, suggesting that NCOA4-mediated ferritinophagy is involved in senescence-induced iron overload and ferroptosis. Furthermore, senescent myoblasts exhibited increased reactive oxygen species (ROS) generation and mitochondrial impairment, which were attributed to cytosolic iron overload-mediated upregulation of mitoferrin 2 (Mfrn2), thereby promoting mitochondria iron import. Finally, pharmacological inhibition of iron overload or ferroptosis by DFO or ferrostatin-1 (Ferr-1) effectively ameliorated skeletal muscle atrophy and functional decline in aged sarcopenia mice. Collectively, these findings elucidate the mechanistic basis of sarcopenia and highlight potential therapeutic avenues targeting iron dysregulation and ferroptosis. - Source: PubMed
Publication date: 2026/08/10
Huang YanQi ZhenChen ChuanYu Zhihua - Oral leukoplakia (OLK) is the most prevalent and extensively studied oral potential malignant disorder (OPMD), with a high risk of progression to malignancy. Ferroptosis has been implicated as a key process in the progression of OLK, and iron metabolism significantly influences the ferroptosis process. DIRAS2, a member of the GTPase family within RAS proteins, is associated with ferroptosis, however, how DIRAS2 affects iron metabolism remains unknown. - Source: PubMed
Publication date: 2026/08/15
Tian ZitongLi XingWang AnyiLi WenjingWang MinTang XiaofeiZhang Min - Bisphenol A (BPA), a widespread environmental endocrine disruptor, is associated with neurodevelopmental disorders and induces oxidative neurotoxicity. Ferroptosis, an iron-dependent cell death driven by lipid peroxidation, has been implicated in toxicant‑induced neuronal injury. However, whether BPA triggers neuronal ferroptosis through autophagy remains unclear. Using HT‑22 hippocampal neuronal cells as an in vitro model, we investigated the role of autophagy‑dependent ferroptosis in BPA neurotoxicity. BPA exposure caused oxidative damage and mitochondrial ultrastructural abnormalities. It also induced ferroptosis‑related changes, including increased malondialdehyde (MDA), prostaglandin endoperoxide synthase 2 (PTGS2) protein expression, and reactive oxygen species (ROS), as well as decreased glutathione (GSH), glutathione peroxidase 4 (GPX4), and solute carrier family 7 member 11 (SLC7A11). These effects were reversed by the ferroptosis inhibitors ferrostatin-1 (Fer-1) and deferoxamine (DFO). Pharmacological inhibition of autophagy with chloroquine (CQ) also reversed BPA-induced GPX4/SLC7A11 downregulation and PTGS2 upregulation. Notably, BPA decreased the expressions of nuclear receptor coactivator 4 (NCOA4) and ferritin heavy chain 1 (FTH1), which was blocked by CQ. Knockdown of NCOA4 attenuated BPA-induced FTH1 and GPX4 loss, and PTGS2 elevation, indicating that NCOA4-mediated ferritinophagy is required for BPA-induced ferroptosis. Mechanistically, BPA activated AMPK/ULK1 axis while inhibiting mTOR; silencing of AMPK or ULK1 partially abrogated BPA-induced autophagy and ferroptosis. Collectively, these findings demonstrate that BPA activates the AMPK/mTOR/ULK1 signaling pathway to promote NCOA4‑mediated ferritinophagy, leading to ferroptosis in HT‑22 cells. This study provides a novel insight into the molecular mechanisms underlying BPA-associated neurotoxicity. - Source: PubMed
Publication date: 2026/08/19
Zhang YueWang YuxinHe PingLiu QilingHan HaijunZhang XuyuanWang Chong - Microplastics (MPs) contamination is widespread and continues to increase. Compared to terrestrial organisms, mallards as waterfowl are more susceptible to MPs exposure. Lycium barbarum polysaccharides (LBP) are bioactive compounds extracted from goji berries; however, the mechanism by which LBP alleviates polyvinyl chloride microplastics (PVC-MPs)-induced renal damage in ducks remains unknown. In this study, network pharmacology was utilized to identify target proteins of LBP against PVC-MPs-induced renal injury. Analyses of protein-protein interaction (PPI) networks, drug-disease-target networks, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment identified 107 key targets, with core targets predominantly enriched in the nuclear factor erythroid 2-related factor 2 (NRF2) signaling pathway. Male mallard ducks were divided into four groups: control, PVC-MPs (10 mg/kg in diet), LBP (50 mg/kg gavage), and PVC‑MPs + LBP. Our results indicate that PVC-MPs significantly reduced kidney weight and organ coefficient while elevating renal injury biomarkers. PVC-MPs also induced pathological damage and interstitial fibrosis, disrupted redox homeostasis (characterized by increased MDA and decreased GSH/CAT), and suppressed the NRF2/Kelch-like ECH-associated protein 1 (KEAP1) pathway. Furthermore, PVC-MPs caused renal iron accumulation and ferroptosis (reduced GPX4 and FTH1, increased ACSL4), along with activation of nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy (elevated LC3, ATG5, NCOA4, and autophagosome formation). Notably, LBP treatment significantly reversed all these effects. In conclusion, LBP alleviates PVC-MPs-induced renal ferroptosis and fibrosis by attenuating NCOA4-mediated ferritinophagy. This study provides novel insights into the nephrotoxic mechanisms of PVC-MPs and supports the development of LBP as a protective feed additive in poultry farming. - Source: PubMed
Publication date: 2026/07/23
Chen YanLi SifanXue YazhenQin XianghongXiong LinWang ZehaoYu ZhiliMa YonggangTong XishuaiJin HaiboLiu WeiZhao HongyanGu JianhongYuan YanBian JianchunLiu ZongpingZou Hui