NDUFA3 Antibody
- Known as:
- NDUFA3 Antibody
- Catalog number:
- csb-pa015624ea01hu
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- CusAb
- Gene target:
- NDUFA3 Antibody
Related genes to: NDUFA3 Antibody
- Gene:
- NDUFA3 NIH gene
- Name:
- NADH:ubiquinone oxidoreductase subunit A3
- Previous symbol:
- -
- Synonyms:
- B9
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 1996-08-30
- Date modifiied:
- 2015-11-20
Related products to: NDUFA3 Antibody
Related articles to: NDUFA3 Antibody
- Leigh syndrome is an important manifestation of childhood-onset primary mitochondrial disease. Panel sequencing and whole exome sequencing are cost-effective for diagnosing mitochondrial diseases; however, more than half of mitochondrial disease cases remain genetically undiagnosed. This study aimed to demonstrate that combining whole genome sequencing (WGS) and RNA sequencing (RNA-seq) analyses can identify disease-causing variants that would otherwise be missed. - Source: PubMed
Publication date: 2025/12/11
Nakamura KohtaKishita YoshihitoSugiura AyumuOzaki KokoroYatsuka YukikoMatsumoto NaoyukiOkazaki AtsukoProkisch HolgerMaruyama KoichiIwasa HiroyasuMurayama KeiMatsumoto HiroshiOhtake AkiraShiraishi YuichiOkazaki Yasushi - Obesity and neurodegeneration are clinically associated diseases with defective autophagy. However, the genetic, biological, and metabolic underpinnings connecting these diseases are not well-understood. Here we identified a Mitochondria (M) gene-signature that is shared between obesity, and neurodegenerative diseases. We demonstrate that, CEBPB elevates M-gene-signature, to form podosomal belts, and enhance ROS production. Inhibiting autophagy collapses podosomal-belts through macropinocytosis to accumulate vacuoles, lipid-droplets, nuclear Notch-1 (nNICD), DEPTOR, and HBV-polymerase mRNAs. Conversely, hemin counteracts these events and suppresses DEPTOR and HBV-polymerase mRNAs by A-to-I-RNA-editing and nonsense-mediated decay. Furthermore, we CRISPR-engineered the antiviral chromosome-19 miRNA cluster (C19MC) to demonstrate that C19MC-miRNAs augment CEBPB, M-gene-signature, ROS, and recapitulate CEBPB-driven phenotypes, in response to autophagy inhibition. Hemin, or a γ-Secretase inhibitor counteract these phenotypes in CRISPR-C19MC-engineered cells. Therefore, a CEBPB and C19MC-driven M-gene-signature regulates the podosomal belt, lipid droplet, HBV, and DEPTOR mRNA dynamics to genetically link obesity, and neurodegeneration at the cellular level. - Source: PubMed
Publication date: 2025/10/31
Jinesh GoodwinMtchedlidze NinoDevarapalli VarshaAdhikary SantanuLockhart JohnNapoli MarcoIsha IshaReiser MichelleCen LingLiu XiaoxianYoder SeanMesa TaniaFlores ElsaBrohl Andrew - Sleep deprivation (SD) impairs long-term memory, but the molecular mechanisms underlying the impact of sleep loss on memory are poorly understood. Molecular changes driven by SD have thus far focused on transcription and translation. Long non-coding RNAs (lncRNAs), a class of regulatory RNAs, have recently been recognized as an important player in memory research. However, it remains unclear how sleep deprivation modulates the expression of lncRNAs or their targets to lead to memory impairment. In this study, we explored the role of lncRNAs in the disruption of spatial memory caused by SD. We examined a set of synapse-associated lncRNAs that were identified through a transcriptome analysis after SD. Among them, we discovered that the lncRNA Cerox1 is downregulated in dorsal hippocampus following SD, and its levels recover after 2.5 hours of rebound sleep. Sleep is critical for the regulation of metabolism and sleep loss impairs mitochondrial function. Both sleep deprivation and Cerox1 knockdown were found to reduce complex I activity of the mitochondrial electron transport chain. This reduction of complex I activity is linked to the decrease in expression of a subset of complex I subunits including Ndufs1, Ndufs3, Ndufa3 and Ndufs6. Overexpression of Cerox1 has the opposite effect, leading to increased complex I activity. Sleep deprivation reduced ATP levels in the dorsal hippocampus, while Cerox1 overexpression restored it. SD disrupted memory consolidation, and this impairment was rescued when Cerox1 was overexpressed. Cerox1 transcript contains multiple miRNA binding sites that regulate the activity of the lncRNA. Notably, overexpression of Cerox1 transcript lacking miRNA binding sites did not rescue the memory deficit caused by SD. Our findings demonstrated that the impairment of memory consolidation after SD is linked to lncRNA-mediated control of mitochondrial electron transport chain activity essential for sustaining energy requirements. - Source: PubMed
Publication date: 2025/09/29
Ravichandran KarthickKisku PallabiNingchangmi LakhuhongPalanisamy PremkumarStrack StefanAbel TedBanerjee Sourav - High-altitude environments are characterised by extreme conditions, including hypoxia, low temperatures, and intense ultraviolet radiation. Mammals inhabiting these environments have evolved unique adaptive mechanisms, the study of which elucidates survival strategies and evolutionary pathways under extreme conditions. Understanding how native high-altitude animals respond to such environments is highly important. This study investigated the high-altitude adaptation mechanisms of the five-toed jerboa (Orientallactaga sibirica) distributed in Qinghai Province (4229 m) and Hebei Province (498 m), China, through comparative transcriptomic analysis of heart, lung, and kidney tissues. The results revealed greater mRNA transcriptional differences in the lung tissue than in the heart and kidney tissues of high-altitude jerboas, indicating heightened lung sensitivity to high-altitude conditions. In lung tissue, high-altitude jerboas show differential expression of genes related to the Complement and Coagulation cascades, Heme binding, Oxidation-reduction process (such as MASP1, A2M, SERPING1, CD55, FGA, C5AR1, and KNG1), which may be associated with modulating immune functions to mitigate hypobaric hypoxia, intense radiation, and cold-induced damage and reducing thrombosis and inflammation risks. Heart tissue exhibits differential expression of Oxidative phosphorylation and Lipid metabolism genes (such as NDUFC2, NDUFA3, NDUFS4, COX4I2, PAFAH1B3, SGMS2 and PPAR2B), which may help maintain energy equilibrium under hypoxic and cold challenges. Kidney tissue exhibits differential enrichment of pathways such as arachidonic acid metabolism and steroid hormone biosynthesis mediated by genes including CYP4A11, CYP2C29, GPX2, PTGDS, CBR1, and UGT2B31, which may help coordinate vascular regulation, immune response, and oxidative balance to maintain systemic homeostasis. These pathways and genes are differentially enriched and expressed between high-altitude and low-altitude five-toed jerboas, which may be candidates for further functional studies of plateau environmental adaptability. Our findings provide candidate genes and pathways for intraspecies adaptations across microenvironments and highlight the need for further functional validation. - Source: PubMed
Publication date: 2025/10/07
Sun Shan-ShanZhang Hao-TingYan Hai-WenKang Xiao-YuBuren Qi-QigeWang Qian-ChengMing MingFeng Jie-RuZhu NaLi XinLing YuZhang DongWu Xiao-DongYuan ShuaiFu He-Ping - Mitochondrial respiratory chain (RC) dysfunction constitutes the biochemical defect underlining a group of heterogenous clinical presentations known as mitochondrial disorders. NDUFA3 is an accessory subunit of Complex I (CI) and has recently been associated with Leigh Syndrome. However, the genetic evidence is limited and no functional analysis is available on the molecular mechanism. - Source: PubMed
Publication date: 2025/10/02
Sun YuWei XiujuanXiao BingLuo YongfengWang YaLiu RipengZhan YongkunYe XiantaoCai XudongXu ShiyiLyu JianxinFang HezhiYu Yongguo