EVI2A antibody - C-terminal region (ARP33842_P050)
- Known as:
- EVI2A (anti-) - C-terminal region (ARP33842_P050)
- Catalog number:
- arp33842_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- EVI2A antibody - C-terminal region (ARP33842_P050)
Related genes to: EVI2A antibody - C-terminal region (ARP33842_P050)
- Gene:
- EVI2A NIH gene
- Name:
- ecotropic viral integration site 2A
- Previous symbol:
- EVI2
- Synonyms:
- EVDA
- Chromosome:
- 17q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-08-03
- Date modifiied:
- 2008-07-18
Related products to: EVI2A antibody - C-terminal region (ARP33842_P050)
Related articles to: EVI2A antibody - C-terminal region (ARP33842_P050)
- Pancreatic ductal adenocarcinoma (PDAC) is prone to drug resistance and a role for fucosyltransferase 3 (FUT3) is increasingly recognized. The current study investigated the mechanisms by which FUT3 contributes to PDAC. FUT3 expression was analyzed via bioinformatics and validated by immunohistochemistry (IHC). RNA sequencing analysis identified significantly upregulated genes in Gemcitabine (Gem)-resistant cells of PDAC(ASPC-1/Gem). The IC50 values, proliferative capacity, invasive potential, and migratory behavior of ASPC-1/Gem cells were quantitatively assessed using using Cell Counting Kit-8 (CCK-8), 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), wound healing, and transwell assays, respectively. Subcellular localization and autophagy were analyzed by immunofluorescence (IF) and electron microscopy. Molecular interactions and signaling pathways were probed through co-immunoprecipitation (Co-IP), reverse transcription quantitative PCR (RT-qPCR) and Western blotting. A FUT3-knockdown mouse xenograft tumor model was established to assess in vivo tumorigenesis. High FUT3 expression correlated with chemoresistance and poor survival in PDAC patients. FUT3 knockdown suppressed autophagy, progression, and chemoresistance in both cell and animal models, while overexpression reversed these impacts. Mechanistically, FUT3 bound to β-1,3-N-acetylglucosaminyltransferase 3 (B3GNT3) to activate Nuclear Factor-kappa B (NF-κB) signal transduction, driving autophagy, progression and chemoresistance. Our results reveal that FUT3 interacts with B3GNT3 and activates the NF-κB signaling, amplifying autophagic activity to drive PDAC progression and confer chemoresistance. - Source: PubMed
Publication date: 2025/12/09
Jin LeiHan WenjieZou JunweiTang XiaoleiChen PengXie HaoZhou BingQian DaohaiYu Yue - Endometrial cancer (EC) is the most common gynecological malignancy in developed countries, with incidence rates continuing to rise globally. However, the precise mechanisms underlying EC pathogenesis remain largely unexplored. This study aims to prioritize genes associated with EC by leveraging multi-omics data through various bioinformatic methods. - Source: PubMed
Publication date: 2024/11/21
Zhang GuoruiMao SuYuan GuangweiWang YangYang JingyunDai Yuxin - EVI2A has emerged as a significant biomarker in various diseases; however, its biological role and mechanism in kidney renal clear cell carcinoma (KIRC) remains unexplored. We used TCGA and GEO databases to analyze EVI2A gene expression comprehensively and performed pan-cancer assessments. Clinical relevance was evaluated through Kaplan-Meier analysis and ROC curves. The gene's immune relevance was explored through analyses of the tumor microenvironment (TME), Tumor Immune Single-cell Hub (TISCH), immune checkpoints, and immunotherapy sensitivity. Our results indicate that EVI2A expression is upregulated in KIRC, showing correlations with tumor grade and T/N/M stage. EVI2A demonstrates high diagnostic accuracy (AUC=0.906) and predicts poor overall and progression-free survival in KIRC patients. Furthermore, EVI2A expression exhibits significant associations with immunity, including TME scores and specific immune cell types such as Tfh cells, CD4 memory T cells, and CD8+ T cells. Elevated EVI2A expression suggests increased sensitivity to PD-1/CTLA-4 and tyrosine kinase inhibitors. assays confirmed the impact of EVI2A on KIRC behavior, with its knockdown resulting in reduced cell proliferation and migration. In conclusion, our comprehensive analysis identifies EVI2A as a promising biomarker and a novel therapeutic target for intervening in KIRC. These findings hold significant implications for further research and potential clinical applications. - Source: PubMed
Publication date: 2024/10/16
Liu RongLi ShengXiong SituZheng FucunZhan XiangpengZeng JinFu BinXu SonghuiZhu ShaoxingChen R U - Endometrial cancer is the most common malignant tumor of the uterus, but the underlying genetic mechanisms of EC remain unclear. To identify candidate genes and investigate genetic mechanisms for endometrial cancer, we utilized the summary-data-based Mendelian randomization (SMR) method to investigate causal associations between genetic variants, gene expression, DNA methylation, and endometrial cancer. Three main analyses were conducted utilizing cis-expression and methylation quantitative trait loci (eQTLs and mQTLs) as instrumental variables to examine causal relationships with endometrial cancer, and assessing the causal relationship between DNA methylation and gene expression. Data sources included genetic association data from O'Mara et al. eQTL data from the GTEx database, and mQTL data from McRae et al. Analysis involved the HEIDI test to distinguish pleiotropy, SMR analysis with multiple testing correction, and colocalization analysis to assess associations driven by linkage disequilibrium. Functional enrichment analysis was performed by the Metascape tool. Our study showed that three genes, SNX11, LINC00243, and EVI2A, were identified as causally related to endometrial cancer. SNX11 exhibited a positive causal relationship, while LINC00243 and EVI2A showed negative ones. Furthermore, 24 CpG sites were identified as causally related to endometrial cancer, with cg14424631 (CYP19A1) being the most significant. The study revealed common genes implicated in endometrial cancer, gene expression, and methylation sites, with LINC00243 playing a key role. Colocalization analysis confirmed significant causal relationships between LINC00243, SNX11, and endometrial cancer. Enrichment analysis uncovered pathways like interferon gamma signaling enriched in both endometrial cancer GWAS and e/mQTL. These findings shed light on the molecular mechanisms underlying endometrial cancer development. The study identified candidate genes and DNA methylation loci causally associated with endometrial cancer, which are expected to serve as potential targets for treatment. - Source: PubMed
Publication date: 2024/10/14
Qin Lan-HuiYang ChongzeSong RuiChen Pei-YinJiang ZijianXu WeihuiZeng GuanzhenLiao Jin-YuanLong Liling - Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by inflammatory cell infiltration, which can lead to chronic disability, joint destruction and loss of function. At present, the pathogenesis of RA is still unclear. The purpose of this study is to explore the potential biomarkers and immune molecular mechanisms of rheumatoid arthritis through machine learning-assisted bioinformatics analysis, in order to provide reference for the early diagnosis and treatment of RA disease. - Source: PubMed
Publication date: 2024/08/05
Mu Kai-LangRan FeiPeng Le-QiangZhou Ling-LiWu Yu-TongShao Ming-HuiChen Xiang-GuiGuo Chang-MaoLuo Qiu-MeiWang Tian-JianLiu Yu-ChenLiu Gang