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)
- RET gene fusion is one of the key oncogenic drivers in papillary thyroid cancer (PTC). However, the impact of different RET fusion subtypes on clinicopathological features and radioiodine (RAI) avidity in metastatic PTC remains unclear. - Source: PubMed
Publication date: 2026/09/28
Shi KexinZhang XinyueHuang ShuhuiTian TianHuang Rui - Intestinal ischemia/reperfusion (I/R) injury is a life-threatening clinical condition associated with high mortality and limited therapeutic options. Ferroptosis, an iron-dependent form of regulated cell death driven by excessive lipid peroxidation, has emerged as a critical contributor to intestinal I/R injury. Nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy promotes ferroptosis by increasing intracellular iron availability; however, the upstream mechanisms governing this process remain poorly understood. Beclin-1 is a key initiator of autophagy, whereas ubiquitin-specific protease 11 (USP11) regulates protein stability through deubiquitination. Whether USP11 modulates NCOA4-mediated ferritinophagy via Beclin-1 during intestinal I/R injury remains unknown. Here, we investigated the role of the USP11/Beclin-1/NCOA4 signaling axis using a murine intestinal I/R model and an oxygen-glucose deprivation/reoxygenation (OGD/R)-induced IEC-6 cell injury model. Bioinformatic analysis, co-immunoprecipitation (CO-IP), gene knockdown, and rescue experiments were performed to characterize ferritinophagy and ferroptosis. Intestinal I/R injury and OGD/R treatment markedly induced NCOA4-mediated ferritinophagy, accompanied by enhanced lipid peroxidation and characteristic mitochondrial damage, whereas these alterations were reversed by the autophagy inhibitor 3-methyladenine (3-MA) and ferroptosis-specific inhibitor Ferrostatin-1 (Fer-1). Beclin-1 was identified as a critical interacting partner of NCOA4, and its knockdown suppressed ferritinophagy, ferroptosis, and intestinal injury. Mechanistically, USP11 expression was significantly upregulated following intestinal I/R injury and stabilized Beclin-1 through deubiquitination. Conversely, USP11 knockdown enhanced Beclin-1 ubiquitination, reduced its stability, and consequently inhibited NCOA4-mediated ferritinophagy and ferroptosis. Consistently, inhibition of USP11 markedly alleviated intestinal injury both in vivo and in vitro. Collectively, our findings reveal a previously unrecognized USP11/Beclin-1/NCOA4 signaling axis that drives ferritinophagy-dependent ferroptosis during intestinal I/R injury. By promoting Beclin-1 deubiquitination and stabilization, USP11 facilitates NCOA4-mediated ferritinophagy and subsequent ferroptotic cell death, highlighting USP11 as a promising therapeutic target for intestinal I/R injury. - Source: PubMed
Publication date: 2026/09/22
Han XiaoxiaMa XiaojieHou MinXing YangWang XinrunLi XiaoxiLiu JieZhou JiaLyu JipengLeng Yufang - Given the established oncogenic role of KRAS in lung cancer and its predicted regulation by hsa-miR-134 and transcription factors (NCOA4, NR3C2, ETS2), we systematically catalogued genetic variation across the KRAS gene. In this study, we identified 21,598 SNPs, of which 475 were missense (2.19%), 580 were synonymous (2.68%), and 18,093 were intronic (83.77%). In silico prioritization combined with cross-validation in TCGA-LUAD and MSK-IMPACT cohorts identified four high-confidence deleterious variants (G13C, G13D, G60S, G60V), confirming the recurrence of G13C/G13D and highlighting the fully conserved switch II residue G60 as a structurally distinctive candidate. In MD simulations, G60S showed the largest conformational displacement (RMSD ≈ 8-9 Å), elevated per-residue flexibility (residues 28-37: 1.90 → 2.99 Å), increased terminal Rg, and reduced hydrogen-bond occupancy, suggesting localized, mutation-specific perturbations within the G-domain. In contrast, G13D maintained near-wild-type dynamics, indicating that functional impairment may not require global structural destabilization. Consistent ensemble analyses (PCA, DCCM, FEL) revealed a dominant single-mode rearrangement for G60S (PC1 ≈ 50.8%), a heterogeneous multi-state landscape for G60V, and a restricted low-energy ensemble for G13D, supporting distinct, position-specific mechanisms. Gene-gene and protein-protein interaction analyses linked KRAS to multiple signaling partners, GO and KEGG enrichment analyses associated KRAS with GTPase activity, Rac protein signaling, and the RAS-MAPK and PI3K-AKT pathways implicated in lung cancer progression. Overall, these findings identify G13C, G13D, G60S, and G60V as high-priority candidates for experimental validation and may inform future strategies for genomic risk assessment and mutation-specific therapeutic intervention in lung cancer. - Source: PubMed
Publication date: 2026/09/25
Mia Md SohelDatta Bimal KumarAkter KhadijaDas Topu Tomal KrishnoShawon Jamima MahzabinHossen FaisulPranto Abdur RahmanShadhin Md Saklain TanverTahsin NowmeeQahl Safa HBakhsh TahaniTalukder Md Enamul Kabir - Mycobacterium tuberculosis (Mtb) increases the availability of free iron, resulting in ferroptosis of macrophages to facilitate its survival and dissemination. A critical factor for elevated levels of labile iron is the overt accumulation of nuclear receptor coactivator 4 (NCOA4), which promotes autophagic degradation of ferritin in a process termed ferritinophagy. Here, we identify a novel post-translational modification on NCOA4 that is essential for its interaction with ferritin in the iron-replete condition of Mtb-infected cells. Specifically, protein arginine methyltransferase 5 (PRMT5) confers symmetric dimethylation on NCOA4, which promotes ferritinophagy-mediated ferroptosis. Using loss-of-function studies, we show that PRMT5 is required for lipid peroxidation, bacterial survival, and dissemination in Mtb-infected mice. Additionally, the overexpression of a methylation-deficient mutant of NCOA4 phenocopies the depletion of PRMT5 and reduces ferritinophagy in Mtb-infected cells. Mechanistically, we identify that PRMT5-mediated methylation enhances the cytoplasmic retention of NCOA4 and reduces its nuclear availability. Thus, our findings uncover the key interaction between NCOA4 and ferritin that regulates ferroptosis and mycobacterial survival during infection. Perturbation of this interaction results in reduced Mtb loads and alleviated disease pathology. - Source: PubMed
Publication date: 2026/09/22
Sundar SmritiRajmani Raju SBalaji Kithiganahalli Narayanaswamy - Nanoplastics are widespread environmental contaminants encountered through ingestion and inhalation, raising concerns about their cardiovascular toxicity. How polystyrene nanoplastics (PS-NPs) disrupt cardiomyocyte iron homeostasis remains unclear. We hypothesized that reduced NLR family member X1 (NLRX1) links PS-NP exposure to stimulator of interferon genes (STING) signaling and nuclear receptor coactivator 4 (NCOA4)-associated iron dysregulation. We examined primary neonatal mouse ventricular cardiomyocytes and an 8-week oral-exposure mouse model. In both models, PS-NPs reduced NLRX1 and glutathione peroxidase 4 (GPX4) protein levels, increased STING phosphorylation and acyl-CoA synthetase long-chain family member 4 (ACSL4) expression, and promoted iron accumulation and lipid peroxidation. Cell viability declined, and mice developed cardiac dysfunction and fibrosis. In cardiomyocytes, NLRX1 mRNA remained unchanged. Bafilomycin A1 attenuated NLRX1 protein loss, while NLRX1 showed greater spatial association with lysosome-associated membrane protein 1 (LAMP1)-positive compartments. NLRX1 overexpression reduced STING phosphorylation, iron accumulation, and lipid peroxidation. STING silencing decreased NCOA4 and increased ferritin heavy chain 1, whereas NCOA4 silencing attenuated GPX4 downregulation and ACSL4 upregulation. Re-expression experiments supported the functional ordering of NLRX1, STING, and NCOA4. Ferrostatin-1 (Fer-1) co-treatment attenuated iron accumulation, lipid peroxidation, and GPX4/ACSL4 changes in both models. It improved cardiomyocyte viability and attenuated cardiac dysfunction and fibrosis, although the myocardial phosphorylated-to-total STING ratio remained above control levels. These findings support ferroptosis-associated cardiac injury following PS-NP exposure, with cellular evidence implicating lysosome-associated NLRX1 protein loss and a downstream STING-NCOA4 response. - Source: PubMed
Publication date: 2026/09/19
Lu GuangzhenWang XiaotingWang XinyeZhuang HongZhou XinZhao Gang