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)
- This study aimed to investigate whether PM2.5 and microplastics (MPs) aggravate ovalbumin (OVA)-induced allergic airway injury and to elucidate the role of mitochondrial dysfunction-associated ferroptosis in this process. An OVA-induced murine asthma model and OVA-stimulated MRE cells were established and exposed to PM2.5 and/or MPs. Histopathological, biochemical, molecular, and functional analyses were performed to evaluate pulmonary injury, oxidative stress, ferroptosis, mitochondrial dysfunction, and inflammatory responses. In addition, OPA1 knockdown and ferrostatin-1 (Fer-1) intervention were used to verify the mechanistic involvement of ferroptosis. Exposure to PM2.5 or MPs further aggravated OVA-induced pulmonary damage, as evidenced by enhanced inflammatory infiltration, increased inflammation score, total cell counts and goblet cell percentage, and impaired lung function. In parallel, co-exposure to PM2.5 and MPs markedly intensified oxidative stress in lung tissue and MRE cells, as shown by increased ROS and MDA levels and decreased T-AOC, CAT, and SOD. Moreover, PM2.5 and MPs enhanced ferroptosis by increasing Fe accumulation, lipid peroxidation, and NCOA4, FTH1, and ACSL4 expression, while suppressing SLC7A11, GPX4, GCLC, and GSS. These effects were accompanied by profound mitochondrial dysfunction, including altered expression of mitochondria-related genes, loss of mitochondrial membrane potential, ATP depletion, reduced mitochondrial respiratory complex activities, impaired oxygen consumption rate, and decreased NADPH and GSH-related antioxidant capacity. Importantly, OPA1 silencing or Fer-1 treatment markedly attenuated PM2.5 +MPs-enhanced ferroptotic and inflammatory injury in OVA-treated MRE cells. Collectively, these findings suggest that PM2.5 and MPs co-exposure may exacerbate allergic airway injury by promoting mitochondrial dysfunction-associated ferroptosis via the OPA1/SLC7A11 pathway. - Source: PubMed
Publication date: 2026/09/16
Ma YucongLiu XidongDiao LeiZhang LuWang FangYu Xiuhua - Diabetes mellitus complicated with depression (T2DD) is different from a single disease. It leads to more severe damage to nerve cells and cognitive dysfunction, and has a poor prognosis. Existing evidence indicates that ferroptosis-a form of programmed cell death driven by iron accumulation and lipid peroxidation-is involved in both diabetes and depression. Glutathione peroxidase 4 (GPX4) and long-chain acyl-CoA synthetase family member 4 (ACSL4) are key regulators of ferroptosis, but their roles in T2DD-associated neural damage remain unclear. - Source: PubMed
Publication date: 2026/08/31
Wang YiWang ShuoZhao ShuaiLei YanliFan YuchengZheng XinyiYang LanMa Yanmei - Spinal cord injury (SCI) is a devastating neurological condition characterized by irreversible primary damage followed by a complex secondary injury cascade involving oxidative stress, neuroinflammation, iron dysregulation, and regulated cell death. Among these mechanisms, ferroptosis, a distinct, iron-dependent form of regulated cell death driven by lipid peroxidation and redox imbalance, is increasingly recognized as a critical mediator of neurodegeneration after SCI. The miRNAs play essential roles in neural injury responses by modulating inflammation, oxidative stress, and cell-death pathways. Growing evidence indicates that miRNAs closely regulate ferroptosis-related signaling networks following SCI, influencing key molecular targets including iron metabolism, antioxidant defense systems, and lipid peroxidation pathways. Conversely, ferroptotic stress may alter miRNA expression profiles, suggesting a bidirectional regulatory relationship. In addition, ferritinophagy, a selective autophagy pathway degrading ferritin via nuclear receptor coactivator 4 (NCOA4), has emerged as an important yet underexplored regulator of intracellular iron homeostasis and ferroptosis susceptibility in SCI. This review systematically summarizes current evidence on the molecular mechanisms linking miRNAs and ferroptosis in SCI, highlights how miRNA-mediated regulation of ferroptosis contributes to neuronal death, glial responses, and impaired regeneration, and discusses emerging therapeutic strategies targeting this axis to promote neuroprotection and functional recovery. By integrating recent experimental findings, we aim to provide mechanistic insight and identify translational opportunities for miRNA- and ferroptosis-based interventions in SCI. - Source: PubMed
Publication date: 2026/08/28
Poongodi RajuYang Tao-HsiangYang Kuender DLin Hsin-ChiehCheng Jen-Kun - Intraductal carcinoma (IDC) of the salivary gland is an uncommon neoplasm frequently associated with RET rearrangements, particularly in the intercalated duct subtype. Although invasive carcinoma ex IDC has increasingly been recognized, most reported cases have demonstrated overtly invasive or high-grade morphology distinct from the associated intraductal component. Herein, we report a case of NCOA4::RET fusion-positive IDC of the parotid gland showing extensive infiltrative growth into adjacent soft tissue despite deceptively low-grade cribriform histomorphology. Tumor cells showed diffuse SOX10 and S100 expression, supporting intercalated duct differentiation, while cribriform nests demonstrated heterogeneous myoepithelial cell preservation, ranging from an intact peripheral layer to its complete absence. Targeted next-generation sequencing identified an in-frame NCOA4::RET fusion. This case expands the morphologic spectrum of invasive carcinoma ex IDC and highlights that unequivocal infiltrative growth may occur despite retention of a deceptively low-grade feature. - Source: PubMed
Publication date: 2026/09/12
Kim MeejeongPark Jun-OokSun Dong-IlLee Youn Soo - Endometriosis (EMs) is a prevalent gynecological disorder. Ferroptosis, known as a novel type of programmed cell death, contributes to EMs pathogenesis by promoting ectopic endometrial migration. This study was designed to investigate ferroptosis-related genes as diagnostic/predictive biomarkers for EMs using bioinformatics. EMs-related datasets were obtained from the Gene Expression Omnibus (GEO) database, while ferroptosis-related data were retrieved from the FerrDb database. Through differential expression analysis (Limma), weighted gene co-expression network analysis (WGCNA), functional enrichment analysis (GO, KEGG, and Metascape), protein-protein interaction (PPI) network analysis, LASSO regression, Random Forest algorithm, immune infiltration analysis, and matrix correlation analysis, miRNA-target gene regulatory network was constructed. Identification of the potential immune-related hub genes and their regulatory miRNAs was performed to develop early diagnostic strategies, prognostic biomarkers, and therapeutic targets for EMs. Bioinformatics analysis revealed 18 differentially expressed genes (DEGs) and 36 WGCNA module genes associated with ferroptosis in EMs. Eleven core genes were identified, and a multi-gene predictive logistic regression model was established. LASSO regression and Random Forest analyses refined the selection to six genes: BRD7, OSBPL9, AGPS, NRAS, PEX12, and NCOA4, with high diagnostic value. CIBERSORT analysis showed that immune microenvironment alterations in EMs may be closely related to these six hub genes. Additionally, three key miRNAs-hsa-mir-125a-5p, hsa-mir-218-5p, and hsa-mir-124-3p-were predicted. The six immune-related hub genes (BRD7, OSBPL9, AGPS, NRAS, PEX12, and NCOA4) and three regulatory miRNAs (hsa-mir-125a-5p, hsa-mir-218-5p, and hsa-mir-124-3p) may serve as promising targets for the early diagnosis, prognostic evaluation, and therapeutic intervention of EMs. - Source: PubMed
Publication date: 2026/09/11
Kadeer BuhaiqiemuWufuer ShaadaitiMaimaitimin AdilaiAblat NuramatjanLi XiaopengChen Zhifang