Ask about this productRelated genes to: NDUFS3 Blocking Peptide
- 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 Blocking Peptide
Related articles to: NDUFS3 Blocking Peptide
- Hyperphosphorylation and aggregation of tau are pathological hallmarks of tauopathies. Mitochondrial dysfunction is also a common feature of tauopathies. The mechanistic link between tau abnormalities and mitochondrial dysfunction and its relationship to the physiological function of tau, however, is unclear. Here, we demonstrate that tau regulates mitochondrial reverse electron transport (RET), which produces excess reactive oxygen species (ROS), reduces the NAD/NADH ratio, and is activated by aging or stress. In flies, mice, and human induced pluripotent stem cell (hiPSC)-derived neurons, tau depletion eliminates stress-induced RET and confers resilience. Mechanistically, tau enters mitochondria and directly interacts with the complex I subunit NDUFS3 to promote RET in a phosphorylation-dependent manner. Elevated RET further drives tau hyperphosphorylation, establishing a self-perpetuating pathological loop. Inhibition of RET ameliorates tau toxicity across species. RET regulation thus represents a previously unrecognized normal function of tau that becomes pathological in disease, providing a therapeutic target for various conditions characterized by tau abnormalities and mitochondrial dysfunction. - Source: PubMed
Publication date: 2026/08/06
Li WenRimal SumanBhurtel SunilYeung LucasLu Benjamin GGrinberg Lea TSpina SalvatoreSillero Maria Inmaculada CobosSeeley William WGuo SuLu Bingwei - Sleep deprivation (SD), together with inevitable stress inherent to conventional SD protocols, can induce oxidative stress and inflammation, thereby increasing the risk of premature death. However, the source and signaling pathways underlying reactive oxygen species (ROS) generation remain unclear. Here, we demonstrate that both mechanical and thermogenetic SD, along with possible stress induced by both protocols, lead to initial ROS accumulation in gut subregions, including the proventriculus (PV) and PV-resident hemocytes, via upregulation of dopamine (DA) biosynthesis. Intriguingly, DA acts unconventionally by activating mitochondrial reverse electron transfer (RET), presumably through modifying interactions between the respiratory complex I proteins NDUFV1 and NDUFS3. RET-ROS elicits hemolymphatic IMD/Relish-mediated antibacterial defense. However, during chronic SD, downregulation of the APOE/D ortholog Neural Lazarillo promotes the recruitment of hemocytes to the central brain and, together with this process, leads to widespread neuronal ROS accumulation in an Alzheimer's disease (AD) fly model. Inhibiting RET or hemocytic DA levels extends the survival of animals under chronic SD. Our work reveals DA-driven RET-ROS in innate immune cells during SD, highlights the pivotal role of a gut-innate immune-brain crosstalk in mediating the effect of SD manipulation on aging and AD pathogenesis, and suggests ways to lessen the consequence of SD, a profound health issue in modern society. - Source: PubMed
Publication date: 2026/07/08
Zhang YanLee Jae-HyukYu ZiqiTao YinruiRimal SumanHe YanziLv LeiLu BingweiPing Yong - Hypothermic machine perfusion (HMP) has been associated with reduced delayed graft function compared with static cold storage (SCS). However, the molecular mechanisms underlying these differences during cold preservation remain incompletely understood. This study compared cold-storage-related biochemical and histological changes in kidneys preserved by HMP versus SCS using a Lewis rat model prior to transplantation. - Source: PubMed
Publication date: 2026/04/07
LeGrand CalebBhattarai DineshSharma AmodMcGraw Madison KGokden NerimanMacMillan-Crow Lee AnnParajuli Nirmala - Individual growth heterogeneity in Litopenaeus vannamei severely constrains aquaculture uniformity and yield, yet the systemic cellular regulatory mechanisms underlying this phenomenon remain elusive. Here, we combined scRNA-seq and weighted gene co-expression network analysis (WGCNA) to systematically compare hemocyte profiles between fast-growing (FG) and slow-growing (SG) groups, to elucidate the cellular and molecular basis of the "growth-immunity trade-off." We identified six major hemocyte clusters and reconstructed a continuous differentiation trajectory spanning from progenitor-like cells (Cluster 5/0) through a high-metabolic biosynthetic transition state (Cluster 1/3) to mature immune effectors (Cluster 2/4). Pseudotime analysis indicated divergent hemocyte distribution patterns between the two groups: FG hemocytes were predominantly enriched near the trajectory origin (Cluster 5), a population characterized by high expression of tissue development-related genes. In contrast, cells from the SG group were shifted toward the intermediate and terminal stages, showing specific enrichment in the energy-demanding "biosynthetic" subpopulation (Cluster 3). Differential expression analysis showed that Cluster 3 cells in the SG group significantly upregulated mitochondrial complex I subunit (Ndufs3), oxidative phosphorylation, the TCA cycle, and ribosome pathways, exhibiting typical characteristics of high immuno-metabolism. WGCNA further uncovered the upstream regulatory networks driving this trade-off: the FG group systematically activated the dark-orange module (centered on IRS1 and CCND1), which synergistically maintains progenitor reserves via mTOR and insulin signaling. Conversely, the SG group showed higher activity of the turquoise module, characterized by aminoacyl-tRNA biosynthesis and the expression of the antimicrobial peptide Crustin in progenitor-like cells, suggesting a stress-associated immune activation state. These findings suggest that slow growth may be associated with a transcriptomic shift from progenitor-like states toward energetically demanding immune-related states, providing a cellular hypothesis for the growth-immunity trade-off in L. vannamei. These findings provide a novel cellular perspective on crustacean growth traits and identify key molecular targets for breeding superior strains that balance disease resistance and growth. - Source: PubMed
Publication date: 2026/06/05
Niu PanpanJiang ShanshanTian CaijuanZhong HaoLiu MianyuKong JieLuan ShengMeng XianhongXing QunLuo KunGao Huan - The leg muscles of poultry are an important source of high-quality protein and key trace elements. Most of the research on muscle development are focused on the embryonic or growth stage, there is relatively little research on the muscle development of chicken from embryonic stage to growth stages. Therefore, in this study, transcriptome sequencing was performed on leg muscle samples from female Huanglang chickens across embryonic (E13, E17) to growth stages (D1, D14, D35). A total of 7,691 differentially expressed genes (DEGs) were identified by comparison in pairs of the ten groups, and the highest number of DEGs was observed between E13 and D35, with 4,645 DEGs. Time-series expression analysis using STEM revealed three distinct expression clusters: cluster I (2,582 genes, downregulated genes), cluster II (1,666 genes, upregulated genes), and cluster III (614 genes, transient upregulation peaking at D1). GO and KEGG enrichment analyses showed that the DEGs were enriched in pathways such as cell cycle and DNA replication (cluster I), metabolic and muscle structure-related pathways (cluster II), oxidative phosphorylation and mitochondrial function (cluster III). Protein-protein interaction network analysis identified hub genes, including CDC45/MCM complex members in cluster I, mitochondrial genes such as CYTB and ND1 in cluster II, and oxidative phosphorylation genes including NDUFS3 and COX5A in cluster III. Transcription factor prediction highlighted KDM5A, KDM5B, PHF8, and SAP30 as key regulators. The RT-qPCR results of seven genes (ACTN2, PDK4, MYOG, MYOD1, MYH1F, MYH1B, and MYF6) were consistent with the RNA sequencing (RNA-seq) analysis. This study is the first to systematically analyzed the leg muscle development mechanisms of local chicken breeds from embryonic stage to early growth stage. It provides a comprehensive transcriptomic resource for understanding leg muscle development in chickens. - Source: PubMed
Publication date: 2026/05/28
Liu XuWang ZihanChen TingLiang HongniYang CanYang HaiDeng Yuying