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 study aimed to investigate mitochondrial gene mutations and expression in peripheral blood mononuclear cells (PBMCs) of systemic lupus erythematosus (SLE) patients, focusing on MT-ND5, and assess expression changes under lipopolysaccharide (LPS), tumor necrosis factor-α (TNF-α), and dexamethasone stimulation. Peripheral blood was collected from female SLE patients. Mitochondrial DNA (mtDNA) from PBMCs was sequenced using the HiSeq PE150 platform. Quantitative reverse transcription PCR and western blotting were used to evaluate mRNA and protein expression of the most frequently mutated mitochondrial genes. Cultured PBMCs were treated with LPS, TNF-α, or dexamethasone to examine regulatory effects. A total of 589 mtDNA mutation sites were detected in SLE patients. Among 13 protein-coding genes, MT-ND5, MT-CYB, MT-CO1, MT-ND4, and MT-CO3 exhibited the highest mutation frequencies. Expression analysis revealed significantly reduced mRNA and protein levels of these genes in SLE PBMCs compared with controls, with further decreases after stimulation with LPS, TNF-α, or dexamethasone. SLE PBMCs display extensive mitochondrial mutations and downregulation of key genes, particularly MT-ND5. Inflammatory and therapeutic stimuli exacerbate this suppression, suggesting mitochondrial dysfunction contributes to SLE susceptibility and progression. - Source: PubMed
Zhang SuiyingHuang XinglanMai JingmingZhang NingWang XingrongZhao XiaoqingDeng YuqiongSun ShubingCheng Xiping - Major depressive disorder (MDD) exhibits a higher prevalence in women, yet the underlying cellular mechanisms for this clinical disparity remain elusive. To investigate sex-specific molecular mechanisms, we profiled sex-specific molecular responses to sub-chronic stress in the mouse hippocampus at single-nucleus resolution. - Source: PubMed
Publication date: 2026/06/24
Liang LiangYuan Yu-PeiChang Chun-LeiZhang JingLiang Chen - Mucin-4 (MUC4), a key membrane-associated mucin of the corneal apical glycocalyx, plays an important role in maintaining corneal epithelial homeostasis and wettability. Dysregulation of MUC4 has been associated with barrier dysfunction and ocular surface inflammation. This study aimed to investigate the physiological regulatory role of MUC4 in human corneal epithelial cells (HCEs) and elucidate its underlying intracellular mechanisms. MUC4 in HCEs was silenced through lentivirus-based shMUC4 pseudovirion transduction. Cell viability was analyzed via CCK-8 reagent. Cell motility was monitored via real-time culture monitoring system. Mitochondrial function was analyzed by Seahorse analyzer. Expressions of associated proteins were determined by immunoblotting. Changes in phosphorylation levels in major signaling pathways were determined by protein arrays. MUC4 increased time-dependently in HCEs. The expression was efficiently silenced by shMUC4 transduction. MUC4 loss suppressed cell viability through increasing caspase-8 and PARP1 as well as decreasing Bcl-2 and Bcl-xL. MUC4 loss promoted cell motility by increasing the phosphorylation of FAK-Y397 and paxillin-Y118. Maximal respiration and spare respiratory capacity were lower in MUC4-silenced HCEs by decreasing expression of key mitochondrial proteins (ATP8, MT-ND1, MT-ND3, MT-ND5, MT-CO2, and MT-CO3). MUC4 loss activated FAK and triggered the activation of MAPK-associated kinases in HCEs. These findings indicated that persistent MUC4 production maintained cell viability and hindered migration in corneal epithelial cells via FAK/MAPK/P38 signaling pathway. - Source: PubMed
Publication date: 2026/05/27
Chen Tsan-ChiWu Wan-LinChang Shu-Wen - Hypospadias is among the most prevalent congenital malformations in male newborns. Despite its clinical significance, the molecular etiology of hypospadias has not extensively characterized. Although environmental exposures, epigenetic dysregulation, and mitochondrial dysfunction have been identified as potential contributing factors, the role of mitochondrial DNA (mtDNA) methylation in the pathogenesis of hypospadias has not been systematically examined. Therefore, this study aimed to investigate the potential involvement of mtDNA methylation in hypospadias and to explore its association with mitochondrial gene expression and oxidative phosphorylation-related pathways. - Source: PubMed
Publication date: 2026/04/22
Yang HongchaoWang JianZhang YoutianWang WeiGuo LiqiongShi ShuhaoZhang ZhenhuaGuan YongCui Hualei - Gut microbiota disturbances and impaired mitochondrial function are both linked with the development of major depressive disorder (MDD). However, little is known about how they interact in MDD. - Source: PubMed
Publication date: 2026/05/20
Guan XuanShen Xiao-LingHao Yan-NiDong Zai-QuanChen Jian-Min