Ask about this productRelated genes to: COX3 antibody
- Gene:
- MT-CO3 NIH gene
- Name:
- mitochondrially encoded cytochrome c oxidase III
- Previous symbol:
- MTCO3
- Synonyms:
- COX3, COIII, CO3
- Chromosome:
- mitochondria
- Locus Type:
- gene with protein product
- Date approved:
- 1989-10-12
- Date modifiied:
- 2015-08-25
Related products to: COX3 antibody
Related articles to: COX3 antibody
- This case report aimed to describe the clinical presentation of a 21-year-old male patient with subacute bilateral painless vision loss, clinically consistent with Leber hereditary optic neuropathy (LHON), a mitochondrially inherited disorder and to investigate the genetic mutations associated with this condition. - Source: PubMed
Ashrafkhorasani MaryamChou BrianSadun Alfredo A - Pronuclear Envelope Breakdown (PNEB) failure is a critical factor contributing to the early developmental arrest of intracytoplasmic sperm injection (ICSI) embryos; however, its molecular mechanism remains inadequately understood. This study aimed to elucidate the core regulatory network underlying PNEB failure occurrence and its impact on embryonic development. Single-cell sequencing was used to identify differentially expressed genes (DEGs) between PNEB‑type two pronuclei (2PN) zygotes and 3PN control zygotes, and weighted gene coexpression network analysis (WGCNA) was performed to identify module genes associated with PNEB failure. The least absolute shrinkage and selection operator was applied to model disease types and screen core genes, thereby establishing a multiomics integration strategy. Reactive oxygen species (ROS) and 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolocarbocyanine iodide (JC-1) fluorescence staining were conducted to analyze oxidative stress and mitochondrial function. A total of 1294 DEGs were identified, including genes involved in the oxidative phosphorylation pathway. Mitochondrially encoded reduced nicotinamide adenine dinucleotide dehydrogenase 1 (MT-ND1) and mitochondrially encoded cytochrome c oxidase III (MT-CO3) were significantly upregulated, whereas genes associated with the DNA repair pathway were downregulated. WGCNA revealed a light-green module strongly associated with PNEB failure (r = 0.89, P = 1.2e - 5). Hub genes, ribosomal protein L10a (RPL10A) and ribosomal protein L38 (RPL38), within this module were implicated in ribosome biogenesis. The PPI network confirmed functional interactions between MT-ND1 and RPL10A, suggesting that dysregulated mitochondrial function and ribosomal assembly are central to PNEB failure. ROS and JC-1 fluorescence staining showed a significant decrease in the JC-1 red/green fluorescence intensity ratio in the PNEB failure group (p < 0.05), while ROS levels were significantly elevated (p < 0.01). This study reveals that mitochondrial metabolic dysfunction and ribosomal assembly abnormalities contribute to PNEB failure, thereby disrupting nuclear envelope stability. Furthermore, it identifies the MT-ND1-RPL10A/RPL38 axis as a potential novel molecular marker for assessing ICSI embryo quality. - Source: PubMed
Wang ChaoyingFang JunnanYang GuangJiang RanJin HaixiaSong WenyanShi SenlinZhai JunWang HuihuiZhang TongweiYao Guidong - River channel development and hydraulic engineering alter natural flow-velocity patterns, subjecting to heightened hydrodynamic stress and energy expenditure in high-flow-velocity habitats. Regulating the molecular regulatory mechanisms underlying their adaptation to high-flow velocities provides a basis for species conservation and habitat optimization. Fish were exposed for 3 days to a normal flow velocity (3 BL/s) or a high flow velocity (33 BL/s) in a controlled circular swimming system that maintained a stable current without a deliberate low-flow velocity refuge; fish at 33 BL/s sustained upstream swimming throughout the exposure. RNA-seq differential expression analysis and GO/KEGG enrichment were performed on harvested skeletal muscle, with key genes validated via qPCR. A total of 78 differentially expressed genes (DEGs) were identified between the high-flow-velocity group and the normal-flow-velocity group, including 55 up-regulated genes and 23 down-regulated genes. GO and KEGG analyses revealed that the DEGs were predominantly enriched in mitochondrial energy metabolism and neural regulation, notably oxidative phosphorylation, and were further linked to FoxO and IL-17 signaling. Compared to the normal-flow-velocity group, the high-flow-velocity group exhibited significant down-regulation of multiple oxidative phosphorylation-related subunits, including , , , , , , , and . Concurrently, stress response-related genes, such as , , and , showed a down-regulation trend. These transcriptional changes are consistent with reduced expression of genes involved in antioxidant defense and cellular protection under high-flow conditions, integrating differential-expression and pathway-enrichment results. This decline correlates with the down-regulation of genes associated with antioxidant and stress regulation. Pathways related to energy metabolism show significant enrichment, suggesting enhanced regulation of energy supply and allocation. This pattern indicates metabolic reprogramming characteristics adapted to high-flow-velocity stress. - Source: PubMed
Publication date: 2026/02/14
Gao XinWan HuiJiang YuxuanQiu LipingJiang ZhongquanMeng ShunlongSong Chao - Cell motility is critical for physiological processes including wound healing. However, high concentrations of motility-promoting agents may suppress cellular migration; this newly observed phenomenon warrants further characterization. - Source: PubMed
Publication date: 2026/02/04
Li Chang-ZhiZhou Hong-JuanChen Jin-DongHuang JieLiu Yi-XiuQian Chao-Nan - Rhabdomyolysis can be due to mitochondrial myopathy, but mitochondrial DNA (mtDNA) pathogenic variants are often overlooked in standard genetic panels. We report a 41-year-old woman with recurrent rhabdomyolysis due to a novel MT-CO3 variant. Muscle biopsy showed cytochrome c oxidase-negative fibers that segregated with high heteroplasmic load on single-fiber. We additionally review previously reported mtDNA variants associated with rhabdomyolysis, highlighting the diagnostic relevance of mtDNA analysis and tissue-specific testing in unexplained rhabdomyolysis. - Source: PubMed
Publication date: 2026/02/08
Barca EmanueleJacoby NuriNaini AliMiller Michael LEmmanuele ValentinaWinfree Christopher JTadesse SabaTanji KurenaiHirano Michio