Ask about this productRelated genes to: NDUFS1 antibody
- Gene:
- NDUFS1 NIH gene
- Name:
- NADH:ubiquinone oxidoreductase core subunit S1
- Previous symbol:
- -
- Synonyms:
- CI-75k
- Chromosome:
- 2q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-04-03
- Date modifiied:
- 2016-10-05
Related products to: NDUFS1 antibody
Related articles to: NDUFS1 antibody
- Atrial fibrillation (AF) contributes to cardiovascular morbidity and mortality. Ubiquitin-specific peptidase 10 (USP10) plays a crucial role in numerous cellular processes; however, its particular role in AF remains largely unexplored. In the present study, USP10 expression was assessed in human atrial samples and angiotensin II-treated (Ang II-treated) mouse atrial tissues. An Ang II-induced AF mouse model was employed to investigate the effects of USP10 on atrial remodeling and AF susceptibility. Calcium imaging and patch clamp techniques were used to evaluate USP10's influence on calcium handling and triggered activity. Additionally, RNA sequencing, coimmunoprecipitation, and ubiquitination assays were performed to explore the regulatory interactions between USP10 and NADH:ubiquinone oxidoreductase subunit S1 (NDUFS1). Our findings demonstrate that USP10 is downregulated in atrial tissues from mouse models and patients with AF. USP10 overexpression counteracts Ang II-induced atrial remodeling and reduces AF susceptibility. Furthermore, USP10 contributes to the restoration of mitochondrial function in AF. Mechanistically, USP10 deubiquitinates NDUFS1 at lysine 621, stabilizing NDUFS1 protein levels and mitigating Ang II-induced mitochondrial dysfunction. This study uncovers a critical mechanistic link between USP10 and NDUFS1. Our findings suggest that upregulating USP10 or targeting NDUFS1 degradation could provide an alternative therapeutic strategy to mitigate AF progression and associated cardiovascular risk. - Source: PubMed
Publication date: 2026/08/24
Fu WanrongTian Xiao-XuZhou JianghuaHuang Yu-XuLi HuanWang ZhenyaWei Tong-You WadeLi LiZhao Guo-Jun - Baiyaozi, the dried tuberous root of Stephania cepharantha Hayata, has long been used in traditional Chinese medicine for acute hepatitis, bacillary dysentery, acute gastroenteritis, abdominal pain, and bleeding disorders, indications that collectively correspond to hepatic inflammation, intestinal mucosal injury, and the bleeding tendency characteristic of cirrhosis-associated intestinal barrier injury. This ethnopharmacological correspondence provides a rationale for evaluating Baiyaozi (Stephania cepharantha Hayata) as a candidate therapy for the cirrhotic intestinal barrier, a setting in which current microbiota-targeted strategies act only indirectly on the intestinal epithelium and no traditional medicine has been shown to act directly on its cell-intrinsic driver, mitochondrial dysfunction. - Source: PubMed
Publication date: 2026/08/12
Zhou YimengSun XuChang Di - Cadmium (Cd) is a widespread environmental pollutant associated with neurotoxicity, but its underlying mechanisms remain unclear. Disulfidptosis is a regulated cell death driven by disulfide stress under conditions of impaired cellular reducing capacity. This study investigated the potential involvement of disulfidptosis-associated molecular alterations in Cd-induced neurotoxicity. Male Sprague Dawley (SD) rats were exposed to cadmium chloride (Low-Dose Group: CdCl: 0.036 mg/kg bw; High-Dose Group: CdCl: 3.6 mg/kg bw) by oral gavage for 30 days. Neurobehavioral performance was assessed using the open field test, elevated plus maze, and Morris water maze. Hippocampal ultrastructure, redox-related metabolites, and disulfidptosis-associated genes were analyzed. In addition, bioinformatics analysis was performed by integrating cadmium-related, neurodegenerative disease-related, and disulfidptosis-related genes. The results showed that high-dose Cd exposure impaired locomotor activity, increased anxiety-like behavior, and disrupted spatial learning and memory ( < 0.05), accompanied by mitochondrial damage in hippocampal neurons. Bioinformatics analysis identified seven overlapping genes and enrichment of ferroptosis and oxidative phosphorylation pathways. Biochemically, cadmium exposure significantly increased the NADP/NADPH ratio ([Control: 1.07 ± 0.044] vs. [High-dose: 3.80 ± 0.059], < 0.05) and decreased the GSH/GSSG ratio ([Control: 2.80 ± 0.059] vs. [High-dose: 1.14 ± 0.091], < 0.05), indicating severe redox imbalance. At the molecular level, cadmium exposure upregulated SLC7A11 mRNA expression by 1.48 ± 0.12-fold ( < 0.01) and SLC3A2 by 1.91 ± 0.55-fold ( < 0.05), while downregulating NDUFS1 expression to 0.84 ± 0.01-fold of control levels ( < 0.01) in hippocampal tissues. These findings suggest that high-dose Cd exposure induced neurotoxicity is associated with mitochondrial dysfunction, redox imbalance, and disulfidptosis-associated molecular alterations. - Source: PubMed
Publication date: 2026/07/16
Wei JingxiaWan JinhaoYuan XinyuSun TianaoMa YongjiePan MinglianZheng ZhanyueZhou YingjieSun Yan - Polycystic ovary syndrome (PCOS) is characterized by reproductive dysfunction, insulin resistance, oxidative stress, and metabolic abnormalities, yet the role of disulfidptosis in granulosa cell injury remains unclear. Here, integrated single-cell and bulk transcriptomic analyses identified granulosa cells as the primary disulfidptosis-associated cell type in the PCOS follicular microenvironment. Disulfidptosis-related genes, including leucine-rich pentatricopeptide repeat-containing protein (LRPPRC), NDUFS1, and OXSM, were significantly downregulated and associated with mitochondrial dysfunction and redox imbalance. A diagnostic model achieved an AUC of 0.867, while Mendelian randomization identified LRPPRC as a protective factor for PCOS. Functionally, LRPPRC deficiency under glucose deprivation induced NADPH depletion, F-actin collapse, and granulosa cell death, which was rescued by 2-mercaptoethanol but not by apoptosis, ferroptosis, or necroptosis inhibitors. , LRPPRC overexpression improved follicular development and hormonal balance in PCOS mice. These findings identify LRPPRC-mediated disulfidptosis as a potential biomarker and therapeutic target in PCOS. - Source: PubMed
Publication date: 2026/07/20
Ling LeleZhang ShiyuZhang DongyaoZhao XueWang JinyangTeng YinchengAi ZhihongZhu Xiaolu - Complex I (CI) deficiency, the most common biochemical defect in pediatric mitochondrial diseases, presents with diverse phenotypes, including cardiomyopathy, myopathy, Leigh syndrome, and mitochondrial leukoencephalopathy (ML). No curative therapies exist. Riboflavin, a precursor of CI cofactors FMN and FAD, is a potential treatment, but evidence is heterogeneous and formal guidelines are lacking. - Source: PubMed
Publication date: 2026/07/13
Ferrera GiuliaInvernizzi FedericaSpagnolo ManuelaLamantea EleonoraMoroni IsabellaArdissone Anna