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)
- Head and neck squamous cell carcinoma (HNSCC) remains a prevalent malignancy with limited therapeutic options. Ferroptosis is an iron-mediated type of programmed cell death, and it has surfaced as a viable oncology treatment approach. Curcumin (Cur) is a natural polyphenol that exhibits potent anti-tumor properties; however, the underlying molecular mechanisms regarding cell death modalities in HNSCC remain underexplored. The results of this study show that Cur is an effective ferroptosis inducer in HNSCC based on transcriptomic sequencing analysis. Cur treatment triggers hallmark ferroptosis characteristics that include iron accumulation, lipid peroxidation, radical oxygen species generation, and mitochondrial damage. These effects are all reversed by the ferroptosis inhibitor ferrostatin-1. Furthermore, we discover that Cur promotes the lysosomal degradation of ferritin heavy chain 1 (FTH1). Specifically, Cur enhances the interaction between the cargo receptor, nuclear receptor coactivator 4 (NCOA4), and FTH1, facilitating ferritinophagy. knockdown blocks FTH1 degradation and rescues HNSCC cells from Cur-induced ferroptosis. These results demonstrate that Cur triggers ferroptosis in HNSCC through NCOA4-mediated ferritinophagy. The results of this study highlight the NCOA4-FTH1 axis as a promising therapeutic target and support Cur as a potential candidate for HNSCC treatment. - Source: PubMed
Publication date: 2026/05/27
Liu YaoNing JunliLi ZegangYang HongLi XinTang ZhangyongShiwu DengZhao YeZhang Ge - Abdominal aortic aneurysm (AAA) lacks effective pharmacotherapy. This study examines whether proprotein convertase subtilisin/kexin type 9 (PCSK9) drives ferroptosis in vascular smooth muscle cells (VSMCs) and whether its pharmacological degradation mitigates disease progression. PCSK9 is enriched in VSMCs of human AAA and in murine models induced by PPE or Ang II. SMC-specific PCSK9 overexpression (PCSK9) increases aortic diameter, aggravates elastin fragmentation and collagen deposition and elevates MMP2/9 expression. Within aortic lesions, PCSK9 enhances iron accumulation and lipid peroxidation while reducing glutathione GPX4, consistent with ferroptosis. In primary VSMCs, PCSK9 overexpression suppresses GPX4 and glutathione, increases malondialdehyde and Fe levels and impairs viability, whereas PCSK9 knockdown attenuates Ang II-induced ferroptosis. Mechanistically, PCSK9 triggers ferritinophagy, as shown by decreased ferritin heavy chain-1 (FTH1) and nuclear receptor coactivator-4 (NCOA4), an increased LC3-II/I ratio and enhanced FTH1-LAMP1 colocalisation. Autophagy inhibition with bafilomycin A1 blocks Fe accumulation and rescues ferroptotic indices. The cell-permeable peptide Cadd4 promotes PCSK9 degradation, restores FTH1 and NCOA4 and suppresses ferroptosis in VSMCs. In PPE and Ang II models, Cadd4 reduces aortic dilation, preserves medial structure and normalises ferroptosis and ferritinophagy markers. PCSK9 drives ferritinophagy-dependent ferroptosis in VSMCs, and Cadd4 represents a promising therapeutic strategy for AAA. - Source: PubMed
Publication date: 2026/06/10
Xia MengdieLi ManChen YanyuChen JialinCui YutingZheng Xi-LongYang JingLi BingzhaoMa XiaofengLiu MiaoFan GangPeng JuanDai XiaoyanTang Zhihan - This study elucidates the role of microglia in ferroptosis and neuroinflammation following ischemic stroke and defines the underlying molecular mechanisms. Single-cell transcriptomic analysis revealed that multiple brain cell types in the MCAO mouse model exhibited ferroptosis-related signatures, with microglia showing the most pronounced changes. Differentially expressed genes in post-stroke microglia were significantly enriched in ferroptosis-associated pathways. Further investigations demonstrated that both in vivo (tMCAO/R) and in vitro (OGD/R-treated microglia) models exhibited marked upregulation of the transcription factor Tbp and the lipid metabolism enzyme Lpl, accompanied by increased expression of pro-inflammatory chemokines CCL2, CCL3, and CCL4. Ultrastructural, biochemical, and molecular analyses confirmed canonical features of ferroptosis, including mitochondrial damage, elevated lipid peroxidation, increased ACSL4 and NCOA4 levels, and reduced GPX4 expression. Mechanistically, Tbp directly bound to and transcriptionally activated the Lpl promoter. Activation of the Tbp-Lpl axis by OGD/R promoted pro-inflammatory polarization and chemokine release in microglia and was associated with exacerbated ferroptotic injury, whereas Tbp knockdown effectively reversed these effects. Collectively, these findings demonstrate that ischemic stroke activates the Tbp-Lpl transcriptional regulatory axis in microglia, coordinately driving lipid metabolic reprogramming, amplifying inflammation, and promoting ferroptosis. This study provides new mechanistic insights into post-stroke neuronal injury and identifies Tbp as a potential therapeutic target for modulating microglial ferroptosis and neuroinflammation. - Source: PubMed
Publication date: 2026/06/10
Wang ZhiqinXiong JieLv Rufeng - The clinical translation of gold(I) pharmacophores for liver cancer is hindered by rapid deactivation, poor tumor selectivity, and off-target toxicity. To address these limitations, we engineered a tumor-targeting bovine serum albumin (BSA)-based nanoarchitecture loaded with a gold(I) complex, designated TEP NPs. As an integrated BSA-gold(I) nanoplatform, TEP NPs inherently induce ferritinophagy and leverage the enhanced permeability and retention (EPR) effect and pH-responsive release for TME-triggered gold(I) delivery. TEP NPs inhibit thioredoxin reductase (TrxR), disrupting redox homeostasis and inducing mitochondrial apoptosis. Simultaneously, TEP NPs activate NCOA4-mediated ferritinophagy, leading to ferritin degradation and a surge in labile iron that synergizes with TrxR inhibition to drive ferroptosis. This trimodal cell death triggers immunogenic cell death (ICD) and DAMPs release. In vivo, TEP NPs reprogram the tumor microenvironment by recruiting immune effectors, establishing a closed-loop of tumor killing and immune activation. - Source: PubMed
Publication date: 2026/06/10
Zhu YejinLi YifeiJiang YumingFan ZhiyueLiu Wukun - Postoperative cognitive dysfunction (POCD) is a common complication in older surgical patients. While its pathogenesis remains unclear, ferroptosis-an iron-dependent form of cell death driven by lipid peroxidation-has emerged as a key mechanism in neurodegeneration. This review proposes that aging creates a ferroptosis-prone environment in the brain through iron dyshomeostasis, impaired antioxidant defenses, and enrichment of polyunsaturated fatty acids, and that surgical trauma and anesthetic exposure may trigger ferroptosis by activating interconnected pathways such as neuroinflammation, blood-brain barrier disruption, and oxidative stress, leading to neuronal injury in cognition-critical regions like the hippocampus. However, the available evidence is largely correlative, and whether ferroptosis acts as a proximal driver of neuronal death or as a late consequence of pre-existing damage remains undetermined. We dissect the core molecular machinery (GPX4, ACSL4, NCOA4, Nrf2) and emerging regulators (MD2/Hepcidin, CPT1A, RUNX1/RBM47/cGAS-STING, miRNAs, mitophagy, gut microbiota-exosome axis). Therapeutic strategies including iron chelators, lipophilic antioxidants, natural products, physical therapies, and nanomaterials are reviewed, but most remain preclinical. Elucidating the role of ferroptosis may open new avenues for early diagnosis, targeted prevention, and effective treatment, provided that causality can be rigorously established. - Source: PubMed
Publication date: 2026/05/22
Jiang DanxiaZhang QiaolanTong YinLou KechengLiu Haicheng