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)
- Cobalt oxide nanoparticles (CoO NPs) are widely used in lithium batteries and semiconductors, and are often detected in water, soil, and occupational environments. While cobalt ions are linked to neurodegenerative diseases, the neurodevelopmental toxicity of CoO NPs remains poorly understood. Ferroptosis, a process regulated by iron homeostasis, can be triggered by ferrous overload through ferritinophagy. This study explores how CoO NPs induce ferritinophagy and their role in neurodevelopmental toxicity. Zebrafish larvae exposed to CoO NPs at concentrations of 0, 5, and 50 mg/L for up to 120 hours post-fertilization (hpf) exhibited dose-dependent developmental toxicity, including delayed hatching, increased malformations, and impaired motor behavior. Transgenic zebrafish models demonstrated neuronal shortening, reduced fluorescence, and altered neurotransmitter profiles, as supported by liquid chromatography-tandem mass spectrometry. CoO NPs induced oxidative stress, leading to iron overload, lipid peroxidation (elevated MDA, depleted glutathione), and ferritinophagy activation, as evidenced by changes in genes and proteins related to iron metabolism (trf, fpn, slc7a11) and ferroptosis (GPX4, ACSL4, FTH1, NCOA4). Ferritinophagy was further confirmed using autophagy inhibitors, demonstrating its role in neurotoxicity. Additionally, Vitamin E (D-α-tocopherol), a lipid-soluble antioxidant that suppresses lipid peroxidation, reduced neurodevelopmental abnormalities, supporting that CoO NP-induced toxicity occurs through ferritinophagy-mediated ferroptosis, leading to neurotransmitter dysregulation. These findings were corroborated in human neuroblastoma cells (SH-SY5Y/SK-N-SH). In conclusion, CoO NPs disrupt iron homeostasis, activate ferritinophagy, and induce ferroptosis, resulting in neurotransmitter dysregulation and neurodevelopmental toxicity. These results provide new insights for assessing the neurodevelopmental toxicity and environmental risk of CoO NPs and similar nanomaterials. - Source: PubMed
Publication date: 2026/08/12
Wang ShaozhuoZhou HaojieTan SiyueGeng ChengyuChen SiyuDeng ZhongxiuShi YifanZhao MengZhao YuzhiWang GaoyuanYuan QitongWang SiruiYang YuxiJiang XinyanWang Shou-LinChen CongWang Chao - Diabetic peripheral neuropathy (DPN) is associated with oxidative stress induced by hyperglycemia. Ferritinophagy is critical for maintaining intracellular iron homeostasis and oxidative injury induced by iron overload. However, the relationship between ferritinophagy and high glucose-induced neuronal oxidative damage has not yet been explored. In this study, we established a model of high glucose-induced oxidative damage in ND7/23 cells. ND7/23 cells treated with rapamycin or bafilomycin A1 were used to investigate changes in ferritinophagy, while cells transfected with NCOA4-siRNA were employed to explore the role of ferritinophagy in this process. The results revealed that hyperglycemia inhibited the viability of ND7/23 cells, increased intracellular iron overload, ROS accumulation, and triggered abnormal ferritinophagy characterized by elevated ferritin, NCOA4, and p62 protein levels, together with a reduced LC3II/I ratio. Activation of ferritinophagy with rapamycin alleviated high glucose-induced iron overload and oxidative injury in ND7/23 cells. In contrast, inhibition of autophagy by bafilomycin A1 exacerbated these high glucose-mediated damages. Intriguingly, we found that NCOA4 knockdown improved high glucose-impaired ferritinophagy, reduced intracellular iron concentration, and mitigated oxidative damage in ND7/23 cells treated with high glucose. In conclusion, we conclude that high glucose inhibits ferritinophagy, disrupts iron homeostasis, thereby leading to intracellular iron accumulation and neuron oxidative stress injury in ND7/23 cells. Our results may provide novel perspectives and potential strategies for the prevention and treatment of high glucose-induced oxidative damage. - Source: PubMed
Publication date: 2026/08/10
Fan KekeJi ZhonghuaLiu Zhongjie - Backgrounddiabetic foot ulcers (DFUs) carry 5-year mortality rates of 50%-70% and recurrence rates of 65% at three to five years. Standard-of-care protocols fail to resolve wound chronicity in a substantial proportion of patients, reflecting incomplete understanding of the cellular mechanisms sustaining non-healing. This narrative review examines trace element dyshomeostasis as a mechanistically distinct driver of ferroptotic cell death across wound-bed cell populations and evaluates targeted therapeutic strategies within this framework.MethodsLiterature was identified through narrative searches of PubMed and Web of Science; emphasis was placed on DFU-relevant experimental models and clinical populations.ResultsLabile iron pool expansion, arising from hemolysis-derived Fe release, vasa nervorum compromise, ferritinophagy dysregulation, and SASP-mediated ferroportin suppression, sustains iron-catalyzed lipid peroxidation across Schwann cells, endothelial cells, fibroblasts, and macrophages. Three upstream metabolic axes, comprising AGEs/RAGE-mediated SLC7A11 suppression, eNOS uncoupling with BH4 depletion, and macrophage iron overload-driven polarization arrest, collectively lower the ferroptotic threshold at the wound margin. AGE-induced ECM stiffening further impairs fibroblast antioxidant capacity via mechanotransduction, while impaired NCOA4-dependent ferritinophagy renders senescent fibroblasts ferroptosis-resistant, sustaining SASP-driven iron retention in neighboring cells. Localized deferoxamine delivery stabilizes HIF-1α and restores angiogenic signaling in preclinical models; selenium supplementation restores GPX4-mediated lipid hydroperoxide clearance. Stimuli-responsive biomaterials coordinating DFO and antioxidant release in response to pathological ROS, MMP, and pH signatures represent a tractable delivery framework.ConclusionIron dyshomeostasis and ferroptosis constitute a therapeutically actionable axis in DFU pathology unaddressed by current standard of care. Large animal model validation and pharmacokinetic profiling in the DFU wound environment remain necessary before clinical translation. - Source: PubMed
Publication date: 2026/08/10
Qin Terry Hao-YuShen SuluAziz AtiqahKamarul TunkuLing Xiu-WenHaseeb AmberZulkifli Eva MahirahTan Han-LingWang Aiden Yi-Fei - The liver represents a primary target organ frequently compromised during the progression of sepsis. Ferroptosis is a distinct mode of regulated cell death driven by iron-dependent lipid peroxidation, which has been identified as being involved in the pathogenesis of sepsis-induced hepatic dysfunction. However, the regulation of ferroptosis in hepatocytes by m6A-modified RNAs under sepsis remains unclear. In this study, we demonstrated that the m6A modification level was markedly increased in septic liver injury, complying with upregulation of the m6A methyltransferase METTL4 and the reader YTHDF1. Further analyses were conducted to explore METTL4-mediated m6A modification in septic mice, and NCOA4 was identified as the target gene. Furthermore, knockdown of NCOA4 ameliorated LPS-induced mitochondrial dysfunction, lipid peroxidation, and liver injury. Accordingly, METTL4-mediated m6A methylation on NCOA4 stabilized its mRNA and facilitated NCOA4-mediated ferritinophagy in LPS-induced THLE-2 cells. As a reader for m6A-modified NCOA4 mRNA, YTHDF1 protein improves the stability of NCOA4. This regulatory axis subsequently accelerates ferroptotic pathways, contributing to the exacerbation of sepsis-associated hepatic impairment. In conclusion, the present study has demonstrated the critical roles of METTL4 in the regulation of ferroptosis in LPS-induced hepatocytes and provides a potential therapeutic target to treat sepsis-induced liver injury. - Source: PubMed
Publication date: 2026/08/09
Luo QiongLi LingJin ZheShen MengmengLi YichengHu LinYang MiaoWang JinZhang Jing - Acupuncture therapy shows promise for polycystic ovary syndrome (PCOS), but its molecular mechanisms remain unclear. This study investigates whether acupuncture alleviates PCOS by regulating granulosa cell (GC) ferroptosis via extracellular vesicles (EVs). - Source: PubMed
Publication date: 2026/07/23
Wu XiaolingLi YuanyinWang NaxinGuo ShuminChen HuilingChen TingyuHuang LianshaZhou Hai