Foxj3 antibody - middle region (ARP31683_P050)
- Known as:
- Foxj3 (anti-) - middle region (ARP31683_P050)
- Catalog number:
- arp31683_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Foxj3 antibody - middle region (ARP31683_P050)
Related genes to: Foxj3 antibody - middle region (ARP31683_P050)
- Gene:
- FOXJ3 NIH gene
- Name:
- forkhead box J3
- Previous symbol:
- -
- Synonyms:
- KIAA1041
- Chromosome:
- 1p34.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-22
- Date modifiied:
- 2014-11-18
Related products to: Foxj3 antibody - middle region (ARP31683_P050)
Related articles to: Foxj3 antibody - middle region (ARP31683_P050)
- The 5' mRNA leader regulates translation through its length and upstream open reading frames (uORFs), but its systematic remodeling in cancer remains unclear. We analyzed isoform-weighted 5' leader features across The Cancer Genome Atlas, the Genotype-Tissue Expression transcriptomes and the Clinical Proteomic Tumor Analysis Consortium proteogenomic cohorts. Tumor-associated shifts frequently opposed normal tissue aging trajectories, with the clearest signals in lung adenocarcinoma and lung squamous cell carcinoma. Raw closed-uORF burden defined the sharpest paired-supported lung cores, whereas residualized closed-uORF burden provided the most stable length-independent signal. Colon adenocarcinoma reproduced the transcriptomic pattern but showed a prominent adjacent-normal field effect, with nontumor colon already shifted toward the tumor pattern relative to healthy colon. Upstream-initiation features did not improve proteome-wide prediction beyond mRNA abundance but showed modest, gene-selective associations within independently prioritized age-opposed lung gene sets. Recurrent proteogenomic anchors included and . These findings define an age-opposed, tissue-dependent pattern of 5' leader remodeling and prioritize specific genes and isoforms for functional investigation. - Source: PubMed
Publication date: 2026/08/18
Pal AyonPal RanavRoy VivekChaki Madhumita GRoy Bhaskar - Alveolar type II epithelial cells (AT2), notable for their high mitochondria content, are essential for maintaining pulmonary homeostasis. However, how mitochondrial function was transcriptionally programmed during AT2 aging remains poorly understood. Here, we used single-cell transcriptome data from 28 healthy human lungs spanning various ages to systematically profile age-related transcriptional changes. Our data suggest that most classical aging markers remained stable with no significant changes during AT2 aging. Using high-dimensional weighted gene co-expression network analysis (hdWGCNA), we identified a gene expression module (M1) that declines during AT2 aging and is enriched for genes involved in mitochondrial respiration. Moreover, by integrating bioinformatic and experimental approaches, we found three transcription factors (TCF7L2, FOXJ3, and TCF7) that play key regulatory roles in controlling expression of mitochondrial respiration-related genes during AT2 aging. Collectively, our findings provide both a transcriptional framework and candidate mitochondria regulators to facilitate future investigation of the causal links between AT2 mitochondrial respiration dysfunction and age-related decline in lung function. - Source: PubMed
Publication date: 2026/06/11
Chen LuHu SiluTang XiaojuWang YujunZou YingLuo FengmingWan Huajing - Sex-determining region Y-box transcription factor 2 ( SOX2) has been implicated in tumorigenesis across various cancers. This study sought to characterize the expression pattern of SOX2 in hepatocellular carcinoma (HCC) and elucidate its potential mechanism in promoting HCC progression by targeting Forkhead box J3 (FOXJ3) and regulating the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway, autophagy, and mitophagy. - Source: PubMed
Publication date: 2026/05/14
Zhang ZhigangRen Wanhua - - Source: PubMed
Publication date: 2026/05/30
Bedrosian Tracy A - High-temperature cooking processes generate oxidized lipids such as 9,10-epoxy stearic acid (ESA), yet its reproductive toxicity remains poorly characterized. Here, we demonstrated that ESA exposure in mice induces hepatotoxicity, reduced serum testosterone, and male reproductive dysfunction, manifested by testicular injury, disrupted spermatogenesis, and impaired sperm quality. Integrated metabolomics and proteomics analysis revealed that ESA disrupts amino acid and carbohydrate metabolic homeostasis, and analysis of these two datasets suggests that mitochondrial dysfunction is likely a key factor in its toxicity. ESA activated the Bax/Bcl-2-mediated mitochondrial apoptotic pathway, leading to increased germ cell apoptosis. In vitro validation in GC-2spd(ts) confirmed that ESA downregulated key mitochondrial-related genes, including Ndufa4l2 and Mettl20, reduced ATP production, suppressed mitochondrial Complex I activity, and induced oxidative stress. ESA also significantly downregulated essential spermatogenesis-related genes, including Cxcr4, Bbof1, Spata25, Sdc1, Rhox5, and Foxj3. These findings establish that ESA impairs male reproductive function through mitochondrial dysfunction, manifesting as impaired energy metabolism, elevated oxidative stress, and activation of the intrinsic apoptotic pathway, alongside suppression of spermatogenesis-regulatory gene networks. This study identifies ESA as a key toxic monomer in oxidized frying oil and underscores the need to incorporate specific lipid oxidation products into food safety assessments. - Source: PubMed
Publication date: 2026/05/26
Huang XinYuan LiyangZhang XinanHe KexuanFan JunjieLiu YunlongWu JianrongChen YueqingRuan HuajuanXu Yong-JiangZhang JianbinYang JunHong Yeting