Ask about this productRelated genes to: NDUFC2 antibody
- Gene:
- NDUFC2 NIH gene
- Name:
- NADH:ubiquinone oxidoreductase subunit C2
- Previous symbol:
- -
- Synonyms:
- B14.5b, HLC-1
- Chromosome:
- 11q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-12-17
- Date modifiied:
- 2015-11-20
Related products to: NDUFC2 antibody
Related articles to: NDUFC2 antibody
- Skin cancers, including basal cell carcinoma (BCC), squamous cell carcinoma (SCC), cutaneous melanoma (CM) and acral melanoma (AM), exhibit profound heterogeneity in clinical behaviour and therapeutic response. However, how tumour-immune ecosystems are remodelled across skin cancer types and disease stages, and how these changes influence immune escape and treatment resistance, remain poorly understood. - Source: PubMed
Huang LingjuanHou HuihuiZhang XiyuanDong LiangShi WenshengLiu MasonSun JiePrakash AnilSong HaoqiuPei ShiyaoLi XinChen XiangMei ShenglinYin Mingzhu - Diabetic heart disease is marked by structural, functional, and molecular alterations in the myocardium. We investigated the effects of exercise training on oxidative phosphorylation-related genes in the diabetic heart. - Source: PubMed
Publication date: 2026/02/02
Shah Iqbal AliIshaq ShahidLee Shin-DaWu Bor-Tsang - 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 - Preeclampsia (PE) is a leading cause of maternal and fetal morbidity that affects 2-8% of pregnancies worldwide, driven by placental dysfunction and systemic inflammation. Growth arrest-specific protein 6 (Gas6) and its receptor AXL play pivotal roles in PE pathogenesis, promoting trophoblast impairment and vascular dysregulation. This study investigated the transcriptomic reversal effects of AXL Receptor Tyrosine Kinase (AXL) inhibition in a Gas6-induced rat model of PE using RNA sequencing (RNA-seq). Pregnant rats were administered Gas6 to induce PE-like symptoms such as hypertension and proteinuria; a subset also received the AXL inhibitor R428. RNA-seq of placental tissues revealed 2331 differentially expressed genes (DEGs) in Gas6-AXLi versus Gas6 (1277 upregulated, 1054 downregulated). Protein-protein interaction networks and Gene Ontology enrichment highlighted upregulated mitochondrial functions, including electron transport chain components (e.g., NDUFC2, COX5A), suggesting enhanced energy metabolism. In the secondary analysis that compared Gas6 to Control, Gas6-upregulated extracellular matrix proteins (e.g., COL4A1, LAMC1) linked to fibrosis were reversed by AXL inhibition, indicating ameliorated placental remodeling. AXL inhibition activated compensatory pathways beyond Gas6 blockade, unveiling novel mechanisms for PE resolution. These findings position AXL inhibitors as promising therapeutics, offering insights into mitochondrial and fibrotic targets to mitigate this enigmatic disorder. - Source: PubMed
Publication date: 2025/08/08
Chou ArcharlieDavidson BenjaminReynolds Paul RPickett Brett EArroyo Juan A - The brain requires a large amount of energy, primarily obtained through glucose metabolism, which appears to be disrupted in various neuropsychiatric disorders. The etiology of neuropsychiatric disorders is complex and involves genetic factors that are slowly being identified. To investigate whether glucose metabolism-related genes are associated with major psychiatric disorders, we conducted secondary analyses using genome-wide association study (GWAS) summary statistics for major depressive disorder (MDD), bipolar disorder (BD), and schizophrenia (SCZ). Based on predefined glucose metabolism pathway genes, we conducted a multi-layer integrative analysis using gene-level approaches including multi-marker analysis of genomic annotation (MAGMA), transcriptome-wide association studies (TWAS) with joint-tissue imputation (JTI), and summary-based Mendelian randomization (SMR). We further explored gene expression patterns across tissues, druggability, and applied gene network analysis to evaluate the interactions. MAGMA identified 1 significant gene for MDD, 19 for BD, and 32 for SCZ, with gene RBKS shared across all three disorders. TWAS-JTI detected 17 and 35 transcriptome-wide significant genes for BD and SCZ, respectively, while SMR prioritized 2 and 9 putatively causal genes. For MDD, no convergent evidence emerged from TWAS-JTI or SMR analyses. Integrated analysis highlighted NDUFS2, NDUFS7, and NDUFC2 in the oxidative phosphorylation pathway as potential therapeutic targets. Finally, gene network analysis highlighted enrichment in mitochondrial respiratory chain complex I biogenesis, NADH dehydrogenase complex assembly, and ATP synthesis. Our results reinforce the role of energy metabolic disturbance in psychiatric disorders, particularly in BD and SCZ. These findings open avenues for targeted therapeutic interventions, warranting further validation across populations. - Source: PubMed
Publication date: 2025/06/11
Zou ShiqiMendes-Silva Ana PaulaDos Santos Fernanda CEbrahimi MahbodKennedy James LGoncalves Vanessa F