NDUFS3 Antibody
- Known as:
- NDUFS3 Antibody
- Catalog number:
- XW-7941
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- NDUFS3 Antibody
Related genes to: NDUFS3 Antibody
- Gene:
- NDUFS3 NIH gene
- Name:
- NADH:ubiquinone oxidoreductase core subunit S3
- Previous symbol:
- -
- Synonyms:
- CI-30
- Chromosome:
- 11p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2016-10-05
Related products to: NDUFS3 Antibody
Related articles to: NDUFS3 Antibody
- Hyperphosphorylation and aggregation of the microtubule-associated protein tau are recognized as pathological hallmarks of tauopathies; however, the biological activity of tau that drives its pathophysiological effects remains poorly understood . Mitochondrial dysfunction is a common feature of tauopathies . Despite this, the mechanistic link between tau abnormalities and mitochondrial dysfunction, as well as its relationship to tau's physiological function, remains unclear. Here, we demonstrate that tau regulates mitochondrial reverse electron transport (RET), which produces excess ROS, reduces the NAD /NADH ratio, and is activated by aging or stress. In flies, mice, and human induced pluripotent stem cells (hiPSC)-derived neurons, tau depletion eliminates stress-induced RET and confers significant stress resistance. Mechanistically, tau enters mitochondria and directly interacts with the mitochondrial complex I (C-I) subunit NDUFS3, enhancing RET activation in a phosphorylation-dependent manner that correlates with tau pathogenicity. Elevated RET further drives tau hyperphosphorylation, establishing a self-perpetuating pathological loop. Blocking tau entry into mitochondria or disrupting tau/NDUFS3 interaction reduces tau-induced RET. Genetic or pharmacological inhibition of RET protects against tau-induced neurodegeneration across species. RET regulation represents a previously unrecognized normal function of tau that becomes pathological in disease, providing a therapeutic target for conditions characterized by tau abnormalities and mitochondrial dysfunction. - Source: PubMed
Publication date: 2026/04/07
Li WenRimal SumanBhurtel SunilYeung LucasLu Benjamin GGrinberg Lea TSpina SalvatoreCobos Sillero Maria InmaculadaSeeley William WGuo SuLu Bingwei - Mitochondrial dysfunction is central to Parkinson's disease (PD), but assessing it in vivo remains challenging. Plasma L1CAM-immunocaptured putative neuron-derived exosomes (NDEs) offer minimally invasive access to brain molecular signatures. This study investigated whether mitochondrial complex (MC) proteins in NDEs are altered in PD and explored their association with clinical features. Plasma putative NDEs were isolated from 28 patients with PD and 33 normal controls (NCs) by L1CAM immunocapture. Levels of mitochondrial subunits-NDUFS3 (Complex I), UQCRC2 (Complex III), MT-CO1 (Complex IV), and ATP5F1A (Complex V)-and the antioxidant enzyme SOD1 were quantified by ELISA. Correlations with clinical severity and diagnostic performance were analyzed. Compared with NCs, PD patients exhibited significantly lower levels of NDUFS3 and UQCRC2 in NDEs (p < 0.05, after FDR correction). NDUFS3, UQCRC2, and SOD1 showed modest inverse correlations with motor symptom severity (R = -0.26). The NDUFS3/UQCRC2 combination yielded an AUC of 0.763 (95% CI: 0.638-0.862) with 100% sensitivity and 51.5% specificity in this exploratory cohort, indicating limited discriminative capacity. These exploratory findings suggest that mitochondrial proteins within plasma putative NDEs may reflect neuronal mitochondrial alterations in PD. The NDUFS3/UQCRC2 combination represents a candidate signature warranting validation in larger cohorts. - Source: PubMed
Publication date: 2026/03/26
Yao YunxiaLi YuanZhao ChunsongYu QianLi QimengMao WeiZhao LifangCai Yanning - Medulloblastoma (MB) is a common central nervous system malignancy in children, and its relationship with lactate metabolism has become an important area of cancer research in recent years, especially in metabolic reprogramming. This study aimed to determine the effects of lactate metabolism-related genes in the biological mechanisms involved in MB. - Source: PubMed
Publication date: 2026/02/25
Wang CeZhang RongLi ShenglanKang ZhuangXia ShaohuaiLi Wenbin - Tendinopathy is a common musculoskeletal disorder that increases the risk of tendon rupture if not properly treated. Current local injection therapies require frequent administration, and no fully effective drug is yet available. Curcumin (Cur) exhibits excellent anti-inflammatory and antioxidant effects, but its poor water solubility and low stability limit its clinical application. To overcome these challenges, this study encapsulated Cur into pluronic F127-based nanomicelles (Cur-F127) to improve its aqueous solubility and stability. Subsequently, the micelles were incorporated into a hydrogel network (Cur-F127&gel) formed by oxidized hyaluronic acid (oxi-HA) and adipic acid dihydrazide (ADH) to achieve sustained release. The resulting Cur-F127 micelles had a particle size of 20.14 ± 0.287 nm, an encapsulation efficiency (EE%) of 89.95 ± 0.60%, and a drug loading (DL%) of 5.57 ± 0.05%. The composite hydrogel possessed a loose, porous three-dimensional network, excellent biocompatibility, and favorable degradation behavior. The system enabled sustained release of Cur for over 20 days without an initial burst. In a rat model of tendinopathy, Cur-F127&gel significantly promoted tendon repair, as evidenced by reduced inflammatory cell infiltration, improved collagen fiber alignment, restored expression of key mitochondrial-related proteins (Ndufs3, Uqcrq, Uqcr10, Atp5mc3), and alleviated oxidative stress damage demonstrated by increased SOD activity and decreased MDA content in tendon tissue, thereby suppressing disease progression. This injectable sustained-release hydrogel system for poorly soluble drugs provides an effective approach for the local, long-acting delivery of Cur and long-term repair of tendinopathy, highlighting its potential value for clinical application. - Source: PubMed
Publication date: 2026/02/07
Wang ShuangWu KeyiSun MeiqiWang XinruiLi JingyingZhang GuorongQiu Zhidong - Growth is a key genetic improvement target in aquaculture. The giant grouper (), the largest and fastest-growing grouper species, is an important aquaculture species and also an ideal male parent in grouper hybrid breeding, such as hulong hybrid grouper ( ♀ × ♂). However, the genetic basis of this rapid growth is unclear. In this study, we established a hulong hybrid grouper self-cross population, observing significant growth segregation. Using Bulked Segregant Analysis (BSA) and RNA-seq on extreme growth groups, we identified a significant growth-related quantitative trait locus (QTL) on chromosome 2, containing 23 candidate genes and 5 growth-correlated non-synonymous SNPs. Transcriptome analysis revealed 4074 differentially expressed genes. Integrating these results, we identified three critical genes: , , and , involved in cell proliferation, embryonic development, and energy metabolism, respectively. Their expression patterns further supported their association with giant grouper's rapid growth. Our findings provide crucial insights into giant grouper growth mechanisms and valuable molecular markers for grouper breeding. - Source: PubMed
Publication date: 2025/12/15
Zeng LeileiWang TongWei QichuangTao YuhaoChang LeyiZhao YanzhaoPan XunranLi YingjieMeng ZiningYang YangLiu Xiaochun