CHCHD8 Blocking Peptide
- Known as:
- CHCHD8 Blocking Peptide
- Catalog number:
- 33r-8507
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- CHCHD8 Blocking Peptide
Related genes to: CHCHD8 Blocking Peptide
- Gene:
- COA4 NIH gene
- Name:
- cytochrome c oxidase assembly factor 4 homolog
- Previous symbol:
- CHCHD8
- Synonyms:
- E2IG2, CMC3
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 2005-09-13
- Date modifiied:
- 2016-11-16
Related products to: CHCHD8 Blocking Peptide
Related articles to: CHCHD8 Blocking Peptide
- The maturation of oocytes is a critical step in mammalian reproduction, involving dynamic regulation of gene expression. Therefore, investigating how gene expression varies during different stages of oocyte maturation is highly important. This study employed single-cell RNA sequencing (scRNA-seq) to analyze bovine oocytes at the germinal vesicle (GV) and metaphase II (MII) stages. The results identified 1787 differentially expressed genes (DEGs) between the two stages, with 1556 genes upregulated and 231 downregulated in the GV stage. Further investigation using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses indicated that the upregulated genes are mainly involved in mitochondrial functions and energy metabolism, whereas the downregulated genes are primarily associated with signaling pathways. Validation through RT-qPCR confirmed that , and were significantly higher in GV-stage oocytes, while , and were notably downregulated. This study highlights significant gene expression differences between GV and MII bovine oocytes, underscoring the vital roles of genes related to energy metabolism and signaling during oocyte maturation. The expression patterns of these genes provide important molecular markers for further elucidating the mechanisms underlying oocyte maturation. - Source: PubMed
Publication date: 2026/04/21
Wang XueyanHuang FeiLi XiaopengHu KaiChen HongNiu PengQu HuiminFang DiHan ChunmeiGao Qinghua - Metastasis remains the leading cause of cancer-related mortality, yet effective interventions against KRAS driven lung adenocarcinoma metastasis ared limited. In this study, using KRAS;TP53;COA4 transgenic mice, clinical specimens, organoid models, RNA sequencing, xenograft assays, and Seahorse metabolic profiling are employed to identify COA4 as an evolutionarily conserved regulator of cytochrome c oxidase (COX) and activator of CDC42. COA4 is found to be highly overexpressed in KRAS mutant tumors, correlating with increased metastatic burden and poor prognosis. Notably, COA4 deficiency markedly reduces lymph node metastasis. Mechanistically, KRAS upregulates COA4 via PI3K signaling and E2F1-mediated transcriptional activation. Functionally, COA4 overexpression enhances transendothelial migration, extravasation, metastatic colonization, and organoid formation in vitro and in vivo, while its knockdown reverses KRAS-driven metastasis without affecting proliferation. Subcellular fractionation reveals that mitochondrial COA4 augments COX activity to drive oxidative phosphorylation, while cytosolic COA4 binds and activates CDC42 to regulate pseudopodia formation. Pharmacological blockade of COX, oxidative phosphorylation, or CDC42 effectively suppressed COA4-driven metastasis, with combination treatments yielding synergistic inhibition. Remarkably, the Saccharomyces cerevisiae COA4 ortholog recapitulates these dual functions, underscoring their evolutionary conservation. These findings establish COA4 as a critical KRAS effector governing metastasis through dual COX-CDC42 modulation, highlighting its therapeutic potential for KRAS-driven malignancies. - Source: PubMed
Publication date: 2025/09/11
Ji XingzhaoZhang WeiyingXue FuyuanZeng JiazhenZhao QinghuaSun XiaomingSun JianZhou HengXu QuanlinMa GuoyuanSun ShengnanWang YingMu QianLiu YiWan Qiang - This study evaluates the robustness of a previously developed calibration model for low-cost ozone sensors, based on the Adaptive Neuro-Fuzzy Inference System (ANFIS). The model was deployed at a different site without retraining. It was tested in Putrajaya, Malaysia, over a 2-month period in 2018 and compared with conventional laboratory-calibrated models for CO and NO₂ sensors. The ANFIS model demonstrated consistently strong performance for the OX-A431 sensor, with R values approaching 0.9 and lower RMSE, confirming its transferability. However, deviations of up to 70 ppb were recorded during high ozone episodes. This may be due to the limited input variables used-namely O₃, NO₂, temperature, and relative humidity-while other influential factors such as co-pollutants or atmospheric pressure were not included. In contrast, laboratory-calibrated models for the CO-A4 and NO₂-A43F sensors exhibited poorer performance (R = 0.13-0.73), indicating low adaptability under field conditions. These findings underscore the importance of field calibration for low-cost sensors and suggest that incorporating additional environmental and chemical parameters may further improve calibration accuracy. This study contributes to the advancement of generalized machine learning calibration frameworks to enable scalable low-cost sensor networks for ambient air quality monitoring. - Source: PubMed
Publication date: 2025/07/31
Alhasa Kemal MaulanaNadzir Mohd Shahrul MohdAli Sawal Hamid MdPutro Wahyu Sasongko - Autoantibodies against mitochondrial-derived antigens play a key role in chronic tissue inflammation in autoimmune disorders and cancers. Here, we identify autoreactive nuclear genomic DNA (nDNA)-encoded mitochondrial gene products () recognized by breast cancer (BC) patients' sera as nonself, supporting a direct relationship of mitochondrial autoimmunity to breast carcinogenesis. Autoreactivity of multiple nDNA-encoded mitochondrial gene products was mapped to protein-coding regions, 3' untranslated regions (UTRs), as well as introns. In addition, autoantibodies in BC sera targeted intergenic sequences that may be parts of long non-coding RNA (lncRNA) genes, including and other putative lncRNA neighbors of the protein-coding genes and . Increasing evidence indicates that lncRNAs play a key role in carcinogenesis. Consistent with this, our findings suggest that lncRNAs, as well as mRNAs of nDNA-encoded mitochondrial genes, mechanistically contribute to BC progression. This work supports a new paradigm of breast carcinogenesis based on a globally dysfunctional genome with altered function of multiple mitochondrial and non-mitochondrial oncogenic pathways caused by the effects of autoreactivity-induced dysregulation of multiple genes and their products. This autoimmunity-based model of carcinogenesis will open novel avenues for BC treatment. - Source: PubMed
Publication date: 2023/03/29
Obaidat DeyaGiordo RobertaKleinbrink Erica LBanisad EmiliaGrossman Lawrence IArshad RooshanStark AzadehMaroun Marie-ClaireLipovich LeonardFernandez-Madrid Félix - Cataracts are the main cause of reversible blindness worldwide. The ageing of the lens caused by ultraviolet B (UVB) radiation is mostly related to oxidative stress (OS). Little is known about whether OS induced by UVB enhances the sensitivity of lens epithelial cells to ferroptotic stress, which may be a new mechanism leading to age-related cataracts (ARCs). - Source: PubMed
Publication date: 2022/12/01
Mi YuWei ChaoqunSun LiyaoLiu HuiruiZhang JiayueLuo JialinYu XiaohanHe JieGe HongyanLiu Ping