Ask about this productRelated genes to: ACSL3 antibody
- Gene:
- ACSL3 NIH gene
- Name:
- acyl-CoA synthetase long chain family member 3
- Previous symbol:
- FACL3
- Synonyms:
- ACS3, PRO2194
- Chromosome:
- 2q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-25
- Date modifiied:
- 2019-03-21
Related products to: ACSL3 antibody
Related articles to: ACSL3 antibody
- Cerebral ischemia-reperfusion injury (CIRI) remains a major cause of neurological disability and lacks effective neuroprotective interventions. Soy isoflavones (SI), phytoestrogens with antioxidant and anti-inflammatory properties, have shown neuroprotective potential. Given that ferroptosis contributes to CIRI pathogenesis and AMP-activated protein kinase (AMPK) regulates redox homeostasis, iron metabolism, and lipid peroxidation, we investigated whether SI protect against CIRI by activating AMPK and inhibiting ferroptosis. - Source: PubMed
Publication date: 2026/04/02
Wu CailianLuo TiantianHuang JinfengMo Ruikang - Pneumonia caused by Klebsiella pneumonia (Kp) poses a significant risk to global public health. Vitamin D may reduce Kp infection risk and improve prognosis through immunomodulation. This study aimed to validate the treatment effects of Vitamin D and explore its regulatory mechanism in Kp-pneumonia. - Source: PubMed
Hu JiajiaLin YushenGuo WanrongZhang JingcongWu BenquanWang Yanhong - - Source: PubMed
Publication date: 2026/04/17
Liang YichengLiang LinchuanDu MinjunLei YangyangGao YushunLi Shanqing - Ferroptosis, a form of regulated cell death, plays a pivotal role in the development and treatment of cancer because of its impact on tumor cell proliferation, differentiation, and resistance to chemotherapy. NT5DC2, a gene associated with ferroptosis, has been identified as a key facilitator of cellular proliferation and metastasis in several cancers. In this study, we found that NT5DC2 is highly expressed in bladder cancer tissues compared with normal tissues and that its expression is correlated with the poor prognosis of bladder cancer patients. Functionally, we demonstrated that NT5DC2 suppresses ferroptosis in bladder cancer cells and promotes malignant tumor progression. Mechanistically, NT5DC2 interacts with ACSL3 and hampers its ubiquitination, thereby improving the stability of ACSL3, a crucial ferroptosis suppressing protein induced by oleic acid in lymph nodes. In addition, rescue assay results indicated that ACSL3 mediated the roles of NT5DC2 in suppressing ferroptosis of bladder cancer cells. Furthermore, we found that the upregulation of ACSL3 by oleic acid treatment was mediated by NT5DC2 as manifested by the observation that silencing of NT5DC2 abrogates this regulatory effect of oleic acid treatment. Collectively, our findings suggest that NT5DC2/ACSL3 plays a critical role in bladder cancer progression and ferroptosis regulation, suggesting that NT5DC2/ACSL3 is a potential therapeutic target for bladder cancer treatment. - Source: PubMed
Publication date: 2026/04/14
Niu ShaoruiYang PangYao YuyangTang XiaofengYang JunZhang FeifeiChen KangmingJiang ChengliZhou YuhaoBai WeiLi LipingZhou YuntongLv Xiao-Bin - Although hypertension (HYP) consistently predicts cognitive decline, the precise pathogenic cascade within the brain remains elusive. Here we interrogated whether the PPARγ/ACSL3 axis governs HYP-elicited hippocampal ferroptosis and consequent cognitive dysfunction. This study aimed to explore the role of the PPARγ/ACSL3 axis in HYP-induced neuronal ferroptosis and cognitive impairment. In the HYP rat model, behavioral tests (Morris water maze and Y-maze tests) demonstrated that rats in the hypertensive group had a significant decline in learning and memory. Mechanistically, the AngII-AT1R axis was found to be activated in the hippocampus, accompanied by typical ultrastructural features of ferroptosis, increased iron accumulation, elevated oxidative stress, and downregulation of PPARγ, ACSL3, and key ferroptosis defense proteins (GPX4, XCT, and FPN1). In vitro, ACSL3 overexpression alleviated AngII-induced neuronal ferroptosis. Furthermore, the PPARγ agonist rosiglitazone attenuated lipid peroxidation and iron overload by transcriptionally upregulating ACSL3, a direct regulatory relationship confirmed by dual-luciferase reporter assay. In conclusion, under hypertensive conditions, BRAS activation inhibits the PPARγ/ACSL3 axis via the AngII-AT1R pathway, aggravates lipid peroxidation and ferroptosis in hippocampal neurons, and ultimately contributes to cognitive decline. This study provides new experimental evidence for the mechanism research and therapeutic target exploration of HYP-related cognitive impairment. - Source: PubMed
Publication date: 2026/03/31
Wu ZhenyuHuo XufangHuang YubingGong TaowuZhao PengchengZhu YuhangZeng Qingfan