COX6B1 Mouse Monoclonal Antibody
- Known as:
- COX6B1 Mouse Monoclonal Antibody
- Catalog number:
- BIN-001340-M01
- Product Quantity:
- 0.05mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- COX6B1 Mouse Monoclonal Antibody
Related genes to: COX6B1 Mouse Monoclonal Antibody
- Gene:
- COX6B1 NIH gene
- Name:
- cytochrome c oxidase subunit 6B1
- Previous symbol:
- COX6B
- Synonyms:
- COXG
- Chromosome:
- 19q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-11
- Date modifiied:
- 2019-04-23
Related products to: COX6B1 Mouse Monoclonal Antibody
Related articles to: COX6B1 Mouse Monoclonal Antibody
- Bacterial plant diseases severely threaten agricultural production, necessitating the development of novel and eco-friendly antimicrobial agents. In this study, two thiadiazole metal complexes were rationally designed using a molecular hybridization strategy. Compound displayed outstanding antibacterial activity against pv (), pv (), and pv () and . disrupted bacterial cell wall integrity and enhanced rice defense enzyme activities, effectively inhibiting proliferation. Integrated proteomic and transcriptomic analyses demonstrated that promoted host mitochondrial respiration and ATP production. Functional experiments revealed that activated the oxidative phosphorylation pathway by enhancing cytochrome c oxidase subunit 6b-1 (COX6b-1) activity. Molecular docking, molecular dynamics simulations, and gene expression analyses further confirmed COX6b-1 as a key mediator. These findings elucidate the molecular basis of -induced resistance and support the development of COX6b-1-protein bactericides. - Source: PubMed
Publication date: 2026/01/07
Li HongdeLi JianzhuanYang TangbingLi JiaoSong BaoanHu Deyu - COX6B1 is a nuclear-encoded subunit of the human mitochondrial cytochrome c oxidase (cIV) located in its intermembrane space-facing region. The relevance of COX6B1 in mitochondrial physiopathology was highlighted by the missense pathogenic variants associated with cIV deficiency. Despite the assigned COX6B1 role as a late incorporation subunit, the COX6B1 human cell line KO exhibited a total loss of cIV. To get a deeper insight into the mechanisms driving the lack of cIV assembly or destabilization in the absence of COX6B1, we used the COX6B1 KO cell background to express alternative oxidase and COX6B1 pathogenic variants. These analyses uncovered that the COX6B1 subunit is indispensable for redox-sensitive early cIV assembly steps, besides its contribution to the stabilization of cIV in the late assembly stages. In addition, we have evidenced the incorporation of partially assembled cIV modules directly into supercomplex structures, supporting the "cooperative assembly" model for respiratory chain biogenesis. - Source: PubMed
Publication date: 2025/12/17
Čunátová KristýnaVrbacký MarekKnězů MichalPecinová AlenaAlán LukášHouštěk JosefFernández-Vizarra ErikaMráček TomášPecina Petr - Idiopathic pulmonary arterial hypertension (IPAH) is a progressive and devastating disorder. Mitochondrial oxidative stress has been found to be involved in PAH development. This study aims to explore potential mitochondrial oxidative stress-related biomarkers in IPAH via integrated bioinformatics, validate these genes in MCT-induced rat PAH model and examine the functional roles of COX6B1 and HMGCL in mitochondrial oxidative stress in PDGF-induced pulmonary arterial smooth muscle cells (PASMCs). GSE15197 was downloaded from GEO database. Genes associated with mitochondria and oxidative stress were obtained from Molecular Signatures Database and MitoCarta3.0 databases. Weighted gene co-expression network analysis (WGCNA) was used. GO and KEGG enrichment analysis were utilized. Furthermore, machine learning algorithms (LASSO, SVM-RFE and RF) were constructed to screen hub genes. A nomogram model based on the hub genes were performed for evaluation the diagnostic value, and the expression of hub genes were validated by real-time quantitative PCR and Western blot in MCT-induced rat PAH model. Finally, COX6B1 and HMGCL specific siRNAs were transfected into PDGF-induced PASMCs, mitochondrial ROS (mtROS) level and MnSOD activity were examined. A total of 18 genes related to mitochondrial oxidative stress were identified in IPAH. Two hub genes (COX6B1 and HMGCL) were finally determined as potential biomarkers. Based on the 2 genes, a nomogram model was constructed. This model exhibited remarkable diagnostic efficiency values for IPAH. The expressions of COX6B1 and HMGCL were found to be upregulated in MCT-induced PAH model, in agreement with the findings of bioinformatics analysis. While, transfection with either COX6B1 siRNA or HMGCL siRNA suppressed the abnormal accumulation of mtROS and restored MnSOD activity in PDGF-induced PASMCs. Our results indicated that two mitochondrial oxidative stress-related genes (COX6B1 and HMGCL) were identified as diagnostic biomarkers and may serve as potential targets for IPAH development, although further research is necessary. - Source: PubMed
Publication date: 2025/12/09
Zhu YantingWang XiaomingYan XiaohuiSun YanWang QiongZhai Cui - Considering the distinct etiological pathways and molecular characteristics of different lung cancer subtypes, it is crucial to develop subtype-specific prevention strategies and therapeutic targets. This study aimed to identify protein biomarkers and potential therapeutic targets for specific subtypes of lung cancer by integrating population-based observational studies and Mendelian randomisation (MR) analyses. The cohort study was conducted in the UK Biobank, including about 47,000 participants whose blood samples were measured for 2,923 unique proteins and who were followed for the development of lung cancer. Two-sample MR was performed leveraging publicly available data from genome-wide association studies (GWAS) and protein quantitative trait loci (pQTL). Proteins were prioritised based on consistent associations across logistic regression, MR, transcriptomic validation and sensitivity analyses. Tier 1 proteins passed all evaluations, including GP1BA (squamous cell carcinoma) and ACADSB (small cell carcinoma). Tier 2 proteins, supported by transcriptomic evidence but not sensitivity analyses, included AGRN, ITGB2, SEPTIN3 (adenocarcinoma) and DPP10 (squamous cell carcinoma). Tier 3 proteins, supported by logistic regression and MR only, included CD5L, GNPDA, ACAN, C7, DMP1, HEPH, CEACAM6, COX6B1, CPXM2 and IL12RB2. Druggability evaluation suggests that existing drugs targeting ITGB2, GP1BA, ACADSB and COX6B1 could potentially be repurposed for the treatment of specific lung cancer subtypes. - Source: PubMed
Sun WenLiu JingyangLi JiayanLi NingZhang XiaoyuLi ChangweiZhang LiHe YanWu LijuanWang XiaoJi JianguangZheng Deqiang - To resolve the ambiguous causal relationship between sleep disturbances and neurodegenerative diseases such as Alzheimer's disease (AD), we conducted a multi-stage genetic and multi-omics investigation. Our large-scale bidirectional Mendelian randomization analysis identified a robust, asymmetrical pattern of genetic association, providing strong genetic evidence suggesting that liability for neurocognitive decline and AD is associated with sleep disturbances, with substantially weaker evidence for the reverse direction. To identify the underlying molecular drivers, a multi-omics Summary-data-based MR (SMR) analysis prioritized high-confidence causal genes, including , , , and . The predictive power of this gene signature was confirmed using machine learning models (ROC-AUC > 0.8), while functional validation through bulk and single-cell transcriptomics uncovered profound, cell-type-specific dysregulation in the AD brain, most notably opposing expression patterns between neurons and glial cells (e.g., was upregulated in excitatory neurons but downregulated in glia). Functional enrichment and network analyses implicated two core pathways-nucleotide metabolism centered on and synaptic function involving -and our investigation culminated in the identification of a promising therapeutic interaction, with molecular docking validating high-affinity binding between Ecdysterone and COX6B1 (docking score = -5.73 kcal/mol). Collectively, our findings strengthen the evidence that sleep disruption as a likely consequence of neurodegenerative processes and prioritize a set of validated, cell-type-specific gene targets within critical pathways, offering promising new avenues for therapeutic development. - Source: PubMed
Publication date: 2025/11/20
Du YananXia Xiao-YongNi ZhuFan Sha-ShaHe JunwenHe YangMeng Xiang-YuWang XuXu Xuan