Ask about this productRelated genes to: UQCRB antibody
- Gene:
- UQCRB NIH gene
- Name:
- ubiquinol-cytochrome c reductase binding protein
- Previous symbol:
- UQBP
- Synonyms:
- QP-C, QCR7, UQCR6
- Chromosome:
- 8q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-20
- Date modifiied:
- 2016-10-05
Related products to: UQCRB antibody
Related articles to: UQCRB antibody
- Chronic heat stress (CHS) disrupts broiler breast muscle physiology homeostasis, yet the underlying molecular mechanisms remain unclear. In this study, 144 male Arbor Acres broilers (28 d old) were randomly allocated into 3 treatment groups: the normal control (NC) group (22 °C, ad libitum), the heat stress (HS) group (22 °C, ad libitum), the pair-fed (PF) group (22 °C, feed matched to HS). After two weeks of CHS, the HS group exhibited elevated ROS production, increased antioxidant enzyme activities (GSH-Px, CAT, SOD), and higher MDA and carbonyl levels, accompanied by pronounced ultrastructural damage in mitochondria and myofibrils. Metabolic analyses revealed enhanced glycolysis, suppressed lipolysis and oxidative phosphorylation, and reduced ATP and ADP levels, indicating impaired energy homeostasis. CircRNA sequencing identified 61 differentially expressed circRNAs independent of feed intake, which were associated with metabolic regulation, oxidative stress response, and cell growth and apoptosis. GO and KEGG enrichment analyses of parental and target genes implicated key pathways, including peroxisome, glycolysis/gluconeogenesis, HIF-1 signaling, and apoptosis. ceRNA network analysis revealed critical circRNA-miRNA-mRNA axes regulating ROS generation and metabolic adaptation under CHS, such as novel_circ_004536/gga-miR-10c-5p/CYP1C1 and novel_circ_003382/gga-miR-34a-5p/UQCRB. These findings highlight the regulatory role of circRNAs in CHS-induced oxidative stress and metabolic dysregulation in broiler breast muscle, providing potential molecular targets to mitigate heat-induced muscle damage and improve meat quality in poultry. - Source: PubMed
Publication date: 2026/04/27
Liu ZhenLiu YingsenXing TongZhang LinZhao LiangGao Feng - Gliomas are highly invasive brain tumors in which metabolic reprogramming plays a pivotal role in tumor initiation and progression. METTL17, a mitochondria-associated methyltransferase, has been reported to enhance oxidative phosphorylation (OXPHOS) through mitochondrial RNA methylation; however, its function and regulatory mechanisms in glioma remain poorly understood. In this study, we manipulated METTL17 expression in primary P1 and U251 glioma cells using lentiviral-mediated knockdown and overexpression approaches. METTL17 depletion significantly suppressed cell proliferation, migration, and invasion, reduced ATP production and mitochondrial membrane potential, and increased reactive oxygen species accumulation, whereas METTL17 overexpression reversed these phenotypes. Mechanistically, METTL17 sustained mitochondrial OXPHOS by positively regulating key components of the electron transport chain, including NDUFA2, NDUFS1, SDHB, UQCRB, and MT-CO2. Mass spectrometry and co-immunoprecipitation analyses further revealed that METTL17 interacts with the E3 ubiquitin ligase RNF126, which destabilizes METTL17 through K116-dependent ubiquitination. Additionally, we demonstrate that SIRT5 acts as a desuccinylase for METTL17, removing succinylation at Lys274 and thereby facilitating RNF126-mediated ubiquitination and degradation of METTL17. In vivo xenograft experiments further validated that METTL17 knockdown markedly inhibited tumor growth and enhanced apoptosis. Collectively, these findings identify METTL17 as a critical regulator of mitochondrial function and energy metabolism in glioma and reveal a SIRT5-METTL17-RNF126 axis that governs METTL17 stability, providing new insights into glioma metabolic reprogramming and potential therapeutic targets. - Source: PubMed
Publication date: 2026/04/22
He ChunyanZhang ZixiaoWu XiaokeLin ChangjieJin JieyuNi YongQian YingfengWang Yin - Growing epidemiological evidence suggests a bidirectional relationship between gastroesophageal reflux disease (GERD) and ischemic stroke (IS), yet the shared molecular mechanisms remain poorly characterized. This study aims to identify common biomarkers and elucidate the pathogenic links between GERD and IS using integrative bioinformatics and machine learning approaches. Transcriptomic datasets for GERD (GSE26886 and GSE39491) and IS (GSE22255 and GSE58294) were obtained from the Gene Expression Omnibus. Batch effects were corrected using ComBat, and shared differentially expressed genes were identified via limma. Functional enrichment analyses (gene ontology and Kyoto encyclopedia of genes and genomes) were performed to uncover involved pathways. Key hub genes were selected using 3 machine learning algorithms: least absolute shrinkage and selection operator, support vector machine with recursive feature elimination, and random forest. Diagnostic utility was assessed through receiver operating characteristic curve analysis. We identified 52 upregulated and 57 downregulated differentially expressed genes common to both diseases. Enriched pathways included IL-17 signaling, glycosphingolipid biosynthesis, and PI3K-Akt signaling. Machine learning integration revealed 9 hub genes (FAM46C, FUT4, ODC1, UQCRB, ID2, TSC22D1, IL17RB, AHR, and MGAT4B) with consistent dysregulation in GERD and IS. These genes demonstrated high diagnostic accuracy, with combined area under the curve values between 0.9 and 1.0 across validation cohorts. IL17RB and FUT4 were notably upregulated, suggesting roles in inflammatory and glycosylation pathways. Our findings reveal convergent molecular pathways and potential diagnostic biomarkers linking GERD and IS. The identified hub genes may serve as dual-purpose therapeutic targets aimed at mitigating shared inflammatory and vascular mechanisms. Further experimental validation is needed to confirm their clinical relevance. - Source: PubMed
Huang FangZhang Jie - Reperfusion injury following myocardial infarction (MI) poses a significant challenge, as it can exacerbate heart failure despite being the primary treatment. Adenosine is a promising cardioprotective drug, but its rapid degradation in circulation limits its therapeutic potential. Here, we report the design of self-assembled squalene adenosine nanoparticles (SQAdNPs) as a novel strategy to enhance adenosine's therapeutic potential in MI. In a rat ischemia/reperfusion MI model, it was observed that fluorescent SQAd NPs accumulated in the ischemic myocardium for at least 24 h post-intravenous administration. We evaluated the cardioprotective efficacy of SQAd NPs alone and in combination with antioxidant vitamin E (SQAd/VitE NPs), while assessing the impact of pre- vs post-reperfusion administration. Both nanoparticles' formulations improved cardiac function after 3 months, but only SQAd NPs prevented infarct expansion and adverse left ventricle remodelling with no differences between pre- or post-reperfusion treatment administration. Transcriptome analysis revealed that SQAd NPs upregulated genes linked to calcium signalling (Stac), mitochondrial function, as well as angiogenesis (Uqcrb), and DNA regulation (Ddx49), supporting enhanced cardiomyocyte survival. Functional analysis further indicated activation of pathways involved in cardiac repair, including SCF-KIT and EPH-Ephrin signalling, both associated with myocardial protection. Self-assembled SQAd NPs thus offer a unique therapeutic approach for reperfusion injuries, with enhanced efficacy and reduced side effects. - Source: PubMed
Publication date: 2025/10/30
Saludas LauraGarbayo ElisaAbizanda GloriaDormont FlavioSantamaría EnriquePrósper FelipeCouvreur PatrickBlanco-Prieto María J - Low-grade gliomas (LGG) are a heterogeneous category of brain tumors characterized by a variable clinical course, frequently associated with unfavorable prognosis and therapeutic challenges. Understanding the molecular mechanisms underlying LGG progression is crucial for improving prognosis and therapeutic strategies. This study integrates single-cell RNA sequencing and bioinformatics to explore the role of METCGs (mitochondrial electron transport chain genes) in LGG and construct a predictive model for prognosis, and through in vitro experiments, the feasibility of this model was validated. - Source: PubMed
Publication date: 2025/10/08
Li YangLiu QingSu JunJiang LiangqiLi ZhenPeng Hao