Polyclonal Rabbit ETV7 Antibody
- Known as:
- Polyclonal Rabbit ETV7 Antibody
- Catalog number:
- abx034709
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- Polyclonal Rabbit ETV7 Antibody
Related genes to: Polyclonal Rabbit ETV7 Antibody
- Gene:
- ETV7 NIH gene
- Name:
- ETS variant 7
- Previous symbol:
- -
- Synonyms:
- TEL2, TEL-2
- Chromosome:
- 6p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-19
- Date modifiied:
- 2016-10-05
Related products to: Polyclonal Rabbit ETV7 Antibody
Related articles to: Polyclonal Rabbit ETV7 Antibody
- Resistance to 5-fluorouracil (5-FU) remains a major challenge in the treatment of colorectal cancer (CRC). Here, we identify ETS variant transcription factor 7 (ETV7) as significantly upregulated in CRC tissues and cell lines, with elevated expression associated with poor clinical prognosis. Functional assays demonstrate that ETV7 enhances CRC cell proliferation, invasion, and resistance to 5-FU. Mechanistically, ETV7 transcriptionally upregulates CXCL1, leading to increased neutrophil recruitment and enhanced formation of neutrophil extracellular traps (NETs). The resulting NETs-enriched tumor microenvironment promotes tumor aggressiveness and chemoresistance. Pharmacological inhibition of CXCL1 or degradation of NETs effectively attenuates ETV7-driven malignant phenotypes in vitro and in vivo. Collectively, these findings establish an ETV7-CXCL1-NETs axis that contributes to 5-FU resistance in CRC and suggest that targeting this pathway may improve chemotherapy response. - Source: PubMed
Publication date: 2026/03/31
Mo ShuangXia PeiLv YongruiLiu LeiHe ShujinGao HuabinChen LinWu JianqiangHan AnjiaChen Lixia - Acute myeloid leukemia (AML) is an aggressive hematologic malignancy characterized by the uncontrolled growth of immature myeloid cells, often with a poor prognosis due to therapy resistance. This study investigated the prognostic significance of mutations in AML and their impact on chemotherapeutic drug sensitivity. - Source: PubMed
Publication date: 2026/01/30
Ye WuWu XiaTang YuqianZhang YingDu YiwenYang KunYang YankunGong Yuping - E26 transformation-specific variant transcription factor 7 (ETV7) is implicated in various cancers, but its role in oral squamous cell carcinoma (OSCC) remains undefined. This study explores the clinicopathological significance and molecular mechanisms of ETV7 upregulation in OSCC. - Source: PubMed
Publication date: 2025/07/26
Yong Xiang ZhiDi Li JianTang Yu XingHe Rong QuanLi PingTao Ren ChuanChen Gang - Terminal exhaustion is a critical barrier to antitumor immunity. By integrating and analyzing single-cell RNA-sequencing and single-cell assay for transposase-accessible chromatin with sequencing data, we found that ETS variant 7 (ETV7) is indispensable for determining CD8 T cell fate in tumors. ETV7 introduction drives T cell differentiation from memory to terminal exhaustion, limiting antiviral and antitumor efficacy in male mice. Mechanistically, ETV7 acts as a central transcriptional node by binding to specific memory genes and exhaustion genes and functionally skewing these transcriptional programs toward exhaustion. Clinically, ETV7 expression is negatively correlated with progression and responsiveness to immune checkpoint blockade in various human cancers. ETV7 depletion strongly enhances the antitumor efficacy of CD8 T cells and engineered chimeric antigen receptor T cells in solid tumors. Thus, these findings demonstrate a decisive role for ETV7 in driving CD8 T cell terminal exhaustion and reveal that ETV7 may be a promising target and biomarker for improving the efficacy of cancer immunotherapy. - Source: PubMed
Publication date: 2025/01/13
Cheng JieXiao YifengPeng TingZhang ZijianQin YouWang YuqianShi JiangzhouYan JinxinZhao ZihaoZheng LiangtaoHe ZhijunWang JianweiZhang ZeminLi ChengZhu HaichuanJiang Peng - The alternative splicing of a gene results in distinct transcript isoforms that can result in proteins that differ in function. Alternative splicing processes are prevalent in the brain, have varying incidence across brain regions, and can present sexual dimorphism. Exposure to opiates and other substances of abuse can also alter the type and incidence of the splicing process and the relative abundance of the isoforms produced. The disruption of alternative splicing patterns associated with sex differences and morphine exposure in the prefrontal cortex of a pig model was studied. The numbers of genes presenting one or more significant (FDR-adjusted p-value < 0.05) alternative splicing events were 933 and 1,368 genes when comparing females relative to males and morphine- relative to saline-treated animals, respectively. The sex-dependent opioid effect was most extreme in the contrast between morphine- versus saline-treated males with 1,934 significantly differentially spliced genes. The most frequent and significant alternative splicing type was skipped exon (∼56 % event), followed by retained intron (∼15 % events). The pathways encompassing a significant number of differentially spliced genes included axon guidance, glutamatergic synapses, circadian rhythm, and lysine degradation. Genes in these pathways included ROBO1, SEMA6C, GRIN3A, GRM2, ARNTL, CLOCK, HYKK, and DOT1L. Transcription factors ETV7 and DMAP1 presented a significant number of differentially spliced target genes. The distribution of the genes presenting differential alternative splicing in the axon guidance and circadian rhythm pathways indicates that this regulatory mechanism impacts hubs and peripheral genes. The identification of sexual dimorphism in the effect of morphine across multiple pathways confirms the necessity to explore the effects of drugs of abuse within sex. Altogether, our findings advance the understanding of the response to factors that can impact the activity of excitatory synapses by modulating transcriptional mechanisms that support the plasticity of the prefrontal cortex. - Source: PubMed
Publication date: 2025/01/03
Southey Bruce RSunderland Gloria RGomez Andrea NBhamidi SreelayaRodriguez-Zas Sandra L