Ask about this productRelated genes to: C2orf56 antibody
- Gene:
- NDUFAF7 NIH gene
- Name:
- NADH:ubiquinone oxidoreductase complex assembly factor 7
- Previous symbol:
- C2orf56
- Synonyms:
- PRO1853, MidA
- Chromosome:
- 2p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2007-05-31
- Date modifiied:
- 2015-12-16
Related products to: C2orf56 antibody
Related articles to: C2orf56 antibody
- Topoisomerases are essential for resolving topological stress in DNA during key cellular processes. In human cells, six topoisomerases perform specialized yet overlapping functions to manage these challenges. To investigate their distinct and shared roles, as well as their involvement in DNA damage repair, we conducted a comprehensive analysis of the human topoisomerase-associated protein landscape. Using tandem affinity purification coupled with mass spectrometry, we mapped the protein-protein interaction networks of five human topoisomerases under both normal and stressed conditions. Our analysis identified several key interactions that may regulate topoisomerase function. Notably, TOP1 interacts with PUM3, which undergoes a similar relocalization from nucleoli to nucleoplasm following treatment with a TOP1 poison. In addition, we uncovered novel interactions of TOP3A with NSMCE4A, YTHDC2, and NDUFAF7, as well as a previously uncharacterized interaction between TOP3B and the mitochondrial membrane protein TDRKH (TDRD2). We further examined dynamic changes in these interactomes in response to TOP1 and TOP2 poisons and replication stress, distinguishing between interactions in chromatin and soluble fractions. These findings provide new insights into the regulation and functional coordination of human topoisomerases, offering potential biomarkers or therapeutic targets for topoisomerase inhibitors in cancer treatment. - Source: PubMed
Publication date: 2025/10/01
Zhang HuiminXiong YunChen ZhenChen Junjie - Mutations in mitochondrial-related genes underlie numerous neurodegenerative diseases, yet the significance of most variants remains uncertain concerning disease phenotypes. Several thousand genes have been shown to regulate mitochondria in eukaryotic cells, but which of these genes are necessary for proper mitochondrial function and dynamics? We investigated the degree of morphological disruptions in mitochondrial gene-silenced cells to understand the genetic contribution to the expected mitochondrial phenotype and to identify potentially pathogenic variants like pathogenic mutations in MFN2. We analyzed 5835 gRNAs in a high dimensional phenotypic dataset produced by the image-based pooled analysis platform Raft-Seq. Using the MFN2-mutant cell phenotype, we identified several genes, including TMEM11, TIMM8A, NDUFAF4, NDUFAF7, and NDUFS5 (NADH ubiquinone oxidoreductase-related genes), as crucial for normal mitochondrial dynamics in human U2OS cells. Additionally, we found several missense and UTR variants within the genes SLC25A19 and ATAD3A as drivers of mitochondrial aggregation. By examining multiple features instead of a single readout, this analysis was powered to detect genes which had morphological 'signatures' aligned with MFN2-mutant phenotypes. Reanalysis with anomaly detection revealed other critical genes, including APOOL, MCEE, NIT, PHB, and SLC16A7, which perturb mitochondrial network morphology in a manner divergent from MFN2. These studies show causal links between gene knockouts and gene-specific variants into the assembly or maintenance of mitochondrial dynamics and can hopefully lead to a better understanding of mitochondrial related diseases. - Source: PubMed
Publication date: 2025/08/01
Kremitzki ColinWaligorski JasonBachman GrahamAli Lina MohammedBramley JohnVakaki MariaChandrasekaran VinayPatel PurvaMathur DhruvHime PaulMitra RobiMilbrandt JeffBuchser William - Stress is a primary contributor to fatty liver syndrome (FLS) in chickens. Mitochondrial functionality is pivotal in FLS progression, with diminished supercomplex (SC) formation disrupting electron transport and escalating reactive oxygen species (ROS) production. However, the impact of stress on mitochondrial SC in chicken FLS remains elusive. This study used corticosterone (CORT) to model chronic stress and examined its consequences on mitochondrial performance and SC configuration in both in vivo and in vitro FLS models. Notably, the CORT-treated hepatocytes exhibited elevated triglyceride content ( < 0.05), accompanied by increased mitochondrial ROS ( < 0.01). Moreover, CORT-exposed broilers displayed reduced body weight ( < 0.05) alongside heightened liver-to-body weight ratio ( < 0.01), indicative of liver steatosis with increased triglyceride levels in both liver and plasma ( < 0.01). Mitochondrial alterations in reduced ATP content ( < 0.05). Gene expression analysis revealed enrichment in the mitochondrial respiratory chain pathway, with downregulated mRNA expression of complex I-associated SC assembly factors NADH: ubiquinone oxidoreductase complex assembly factor 5 (), NADH: ubiquinone oxidoreductase complex assembly factor, and translocase of inner mitochondrial membrane domain containing 1 ( < 0.05). Meanwhile, the glucocorticoid receptor (GR) protein level and its specific binding to the gene promoter were reduced in the CORT group ( < 0.01 and < 0.05, respectively), accompanied by a decrease in NDUFAF5 protein expression in liver, primary hepatocytes, and AML12 cells ( < 0.05). GR knockdown in AML12 cells reduced NDUFAF5 protein expression ( < 0.05). Thus, these findings imply that GR-mediated transcriptional regulation of complex I assembly factor NDUFAF5 may influence SC assembly, shedding light on stress-induced FLS mechanisms in broilers. This study reveals the pivotal role of GR-mediated transcriptional regulation in stress-induced FLS in chickens. Chronic stress modeled with CORT disrupted mitochondrial SC assembly, impairing electron transport, elevated ROS production, and liver steatosis. Notably, the downregulation of complex I assembly factors (, , and ) and reduced GR binding to were key mechanisms. These findings provide new insights into stress-driven mitochondrial dysfunction in broiler FLS. - Source: PubMed
Publication date: 2025/05/23
Chen HuiminZhang KeYu HuiGuan ZitingZhao RuqianWu Lei - The mechanism of mitochondria-related genes (MRGs) in childhood allergic asthma (CAS) was unclear. The aim of this study was to find new biomarkers related to MRGs in CAS. - Source: PubMed
Publication date: 2024/05/23
Zhao WeiFang HongjuanWang TaoYao Chao - To screen the differentially expressed proteins in the kidneys of rats exposed to chronic intermittent hypoxia (CIH) based on TMT-PRM technology to identify the potential biomarkers of renal injuries induced by CIH. - Source: PubMed
Wei MChen NLi JLiu DShen SWang FWu RChen Q