ETV7 Antibody - C-terminal (OAAB17893)
- Known as:
- ETV7 Antibody - C-terminal (OAAB17893)
- Catalog number:
- oaab17893
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ETV7 Antibody - C-terminal (OAAB17893)
Related genes to: ETV7 Antibody - C-terminal (OAAB17893)
- 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: ETV7 Antibody - C-terminal (OAAB17893)
Related articles to: ETV7 Antibody - C-terminal (OAAB17893)
- The present study aimed to characterize the immune response, differential gene expression, and functional alterations observed following an in vivo challenge of Classical Swine Fever Virus (CSFV) in crossbred pigs. RNA-sequencing was performed on whole blood samples collected from three pigs before and at 7 days post-infection. A total of 3428 differentially expressed genes (DEGs) were identified, including 970 significantly upregulated and 261 downregulated genes (|log fold change| ≥ 1.5, adjusted p < 0.05). The most prominent DEG was LAMB4, a gene associated with cellular attachment receptors facilitating CSFV binding to porcine cells. Several cytokine-cytokine receptor interaction genes, such as CXCL12, CCL2, CCR1, and IL10RA, were upregulated, indicating a strong activation of innate immune responses. Simultaneously, multiple adaptive immune genes, including CD28, CD83, SLA-DQB1, and IL1A, IL12A, IL26 were downregulated, suggesting viral-mediated suppression of antigen presentation and T-cell signaling. Pathway analysis highlighted the involvement of platelet activation and coagulation cascades during viral evasion. Protein-protein interaction (PPI) analysis revealed a core antiviral module comprising MX1, MX2, ISG15, IFIH1, OASL, IFIT1, and UBE2L6, which are central to interferon signaling and viral restriction. Transcription factors such as ETV7, TOX3, and MSC were upregulated, pointing to immune modulation and possible T-cell exhaustion. Conversely, downregulation of HES1, PRDM6, and MYOG indicated impaired lymphocyte differentiation and tissue repair. Overall, the findings suggest a dual host response to CSFV, with strong innate activation alongside adaptive immune suppression, providing valuable insights for vaccine and therapeutic development. - Source: PubMed
Publication date: 2026/06/25
Singh AyushiKumar AmitKhanna ShivaniDhar PronabLatheef Shyma KUpmanyu VikramadityaAgrawal Ravi KantYadav Ajay KumarUpadhyay AmritanshuChand Devatwal PremDwivedi ShraddhaDutt Triveni - The immunosuppressive tumor microenvironment (TME) serves as a central driver of bladder cancer (BCa) progression and prognosis. While its significance is widely acknowledged, the key cellular subsets that mediate this immunosuppressive state and their core regulatory genes remain incompletely understood. Key immunosuppressive cellular subsets and their signature genes were systematically identified using single-cell RNA sequencing (scRNA-seq) data from BCa samples. A prognostic risk model was then constructed via univariate and multivariate Cox regression analyses, based on bulk RNA-seq datasets and the identified signature genes. The role of SUSD2 was further validated in vitro using qRT-PCR, Western blot, immunofluorescence, proliferation, and invasion assays. Compared with adjacent normal tissues, BCa tissues showed significant enrichment of stromal cells (e.g., epithelial cells, fibroblasts). Among these stromal populations, the proportion of myofibroblast-like cancer-associated fibroblasts (myCAFs) was significantly increased in BCa tissues, and high myCAF infiltration was closely associated with poor patient prognosis. Pseudotime trajectory analysis confirmed that fibroblast differentiation in BCa shifts toward a terminal state (State 3), which is predominantly composed of myCAFs. A prognostic model established using myCAF-related signature genes (TMEM74B, ABCC9, FCMR, ALG9, SUSD2, and ETV7) exhibited stable predictive performance in both training and validation cohorts, with SUSD2 identified as a risk-related gene. In vitro experiments revealed that SUSD2 knockdown inhibited myCAF activation and extracellular matrix secretion, thereby attenuating its promotional effects on BCa cell proliferation and invasion. The TGF-β receptor inhibitor SB-431542could reverse the facilitative effects of SUSD2 overexpression on tumor cell proliferation and migration. Our findings identify myCAFs as a core regulatory cellular subset and SUSD2 as a key molecule within the immunosuppressive TME of BCa. Additionally, SUSD2 may trigger the activation of the TGF-β/Smad signaling cascade to induce myCAF activation, thereby accelerating BCa progression. These results provide novel potential targets and a theoretical basis for prognosis assessment and TME-targeted therapy in BCa. - Source: PubMed
Publication date: 2026/06/19
Song WeihangHan GuangyeLi ZhenhuiHu JunlingMa Kuo - 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 - BACKGROUND: 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 SRSF2 mutations in AML and their impact on chemotherapeutic drug sensitivity. METHODS: The prognostic value of SRSF2 mutations was analyzed in AML patients. SRSF2-mutant cell models were generated via lentiviral transduction for drug sensitivity testing. Xenograft mice were used to assess daunorubicin (DNR) efficacy. Mechanistic studies included transcriptomics, splicing analysis, mRNA stability, polysome profiling, RNA immunoprecipitation, and metabolic assays to identify targetable resistance pathways. RESULTS: Clinical analysis revealed that SRSF2 mutations decreased the survival of AML patients. In vitro experiments demonstrated that SRSF2 mutation reduced the sensitivity of AML cells to drugs such as DNR and homoharringtonine but did not affect the response to venetoclax. In mouse models, DNR treatment was effective against wild-type AML but showed significantly reduced efficacy in suppressing tumors and improving survival in SRSF2-mutant AML. Mechanistically, SRSF2 mutation impaired the interaction between the SRSF2 protein and THBS1 mRNA, prolonging the THBS1 mRNA half-life and enhancing its translation efficiency, leading to THBS1 protein accumulation. Additionally, the mutation altered the splicing pattern of ETV7 and upregulated its expression, potentially mediating DNR resistance. Metabolic analysis revealed that mutant cells presented increased spare respiratory capacity, supporting energy demands under stress. Inhibition of the PDGFB pathway (CP-673451) synergistically enhanced the cytotoxic effect of DNR on mutant cells. CONCLUSIONS: SRSF2 mutations promoted DNR resistance through multiple mechanisms, and targeted combination therapy with PDGFB pathway inhibitors may represent a novel strategy to improve therapeutic outcomes in patients with mutations. - 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