TNK2 Antibody
- Known as:
- TNK2 Antibody
- Catalog number:
- XW-7864
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- TNK2 Antibody
Related genes to: TNK2 Antibody
- Gene:
- TNK2 NIH gene
- Name:
- tyrosine kinase non receptor 2
- Previous symbol:
- -
- Synonyms:
- p21cdc42Hs, ACK, ACK1
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-19
- Date modifiied:
- 2016-04-28
Related products to: TNK2 Antibody
Related articles to: TNK2 Antibody
- Previous clinical studies have reported that not all depressed patients respond to antidepressants. Therefore, finding potential predictive molecular biomarkers is crucial for providing important guidelines in the diagnosis and treatment of depression. In recent years, some studies have identified potential signature molecules using machine learning analysis of transcriptomic data. In this study, we analyzed transcriptomic data from duloxetine-treated depressed patients and used a random forest algorithm to identify a set of characteristic microRNAs and mRNAs. For the mRNA expression dataset, we identified a gene set having 30 transcripts, including TNK2 (Gini index =2.11) and KDM2A (Gini index =1.81), with an AUC value 10-fold and cross-validation equal to 0.907. We also identified the feature microRNA sets (n = 20) with an AUC value of 0.711. Gene annotation function analysis suggests that those feature mRNAs mainly mediate myosin complex and EGFR-related activities. When we explored the relationship between microRNAs and mRNAs, 151 microRNA-mRNA pairs showed negative correlations, while 129 pairs showed positive correlations. Meanwhile, 58 microRNA-mRNA pairs showed potential functional regulatory relationships based on seed-region sequence complementarity. We also confirmed direct regulation between several characteristic microRNAs and mRNAs using luciferase reporter assays. Subsequently, we found that the expression levels of TNK2 (P = 0.0044) and KDM2A (P = 0.0080) were significantly up-regulated after duloxetine treatment of SYSH cells. In a depressive animal model, mice administered with duloxetine showed altered mRNA and protein expression of those feature genes in the prefrontal cortex. Altogether, we identified the signature microRNAs and mRNAs that can distinguish duloxetine-effective and duloxetine-ineffective phenotypes and a close regulatory relationship between signature microRNAs and mRNAs. These characteristic molecular signatures may serve as predictive biomarkers for duloxetine efficacy, enabling patient stratification before and during treatment and providing a theoretical foundation for individualized antidepressant therapy and informed clinical decision-making. - Source: PubMed
Publication date: 2026/04/16
Zhao YanLei ChunguangTao YanlinXiong LanDwivedi YogeshWang Qingzhong - This study focuses on the function and molecular mechanisms of the tyrosine kinase non-receptor 2 (TNK2) in esophageal squamous cell carcinoma (ESCC). In this study, using ESCC as a model, techniques such as Western Blot, immunoprecipitation (IP), Transwell assay, and immunofluorescence staining, combined with lentiviral transfection experiments, were employed to analyze the molecular regulatory mechanism of TNK2. Analysis revealed a marked increase in TNK2 expression levels in clinical ESCC specimens and established ESCC cell lines. TNK2 promoted epithelial-mesenchymal transition (EMT), proliferation, and invasion of ESCC cells. Functional experiments demonstrate that TNK2 promotes EMT, proliferation, and invasive capacity in ESCC cells. Mechanistically, TNK2 interacts with AKT and promotes its phosphorylation, which in turn inhibits the ubiquitination and proteasomal degradation of FOXO1, ultimately leading to increased FOXO1 protein expression. This study reveals that TNK2 enhances FOXO1 expression via the AKT signaling axis, thereby driving ESCC malignant progression. Genipin targets TNK2 to inhibit the progression of ESCC. It provides new insights into the pathogenesis of ESCC and theoretical basis for positioning TNK2 gene as a potential therapeutic target. - Source: PubMed
Publication date: 2025/12/10
Zhou MengyuanYang YongliangQiu TianWu YanZhu WentingXu ZihanLi XinranHuang HongyuMa RuiLu YingzhiDong Zibo - Pancreatic ductal adenocarcinoma (PDAC) remains highly lethal due to its aggressive nature and limited treatment options, with the efficacy of immunotherapy constrained by a uniquely immunosuppressive tumor microenvironment (TME). In this study, we identify TNK2/ACK1 as a key regulator of the immunosuppressive TME in PDAC. TNK2/ACK1 is significantly upregulated in PDAC, at least in part via gene amplification and KRAS-G12 mutations. Mechanistically, TNK2/ACK1 directly phosphorylates and activates STAT5A to induce the expression of the immune checkpoint HVEM, which suppresses CD8⁺ T-cell function via its receptor BTLA. Pharmacologic targeting of TNK2/ACK1 with AIM100 or (R)-9b enhances CD8⁺ T-cell activation and cytotoxicity while reprogramming the TME. Furthermore, combining TNK2/ACK1 inhibitors with anti-PD-1 immunotherapy or with nab-paclitaxel plus gemcitabine demonstrates promising antitumor efficacy in both allograft and spontaneous PDAC models. Overall, our findings reveal a mechanism of immune evasion and provide a potential framework for developing tailored immunotherapeutic strategies in PDAC. - Source: PubMed
Publication date: 2025/12/06
Wu ChaoLiu WeishuaiHu XiangtingXie YongjieLi ShengnanLiu XinyueSun ZhaojunLi XiaolingYu XinYuan YudongZou YipingAn RanChen YananWang HailongFeng YukuanGao SongWang HongweiWang YifeiWang NanYang ChaoYu JunSun PeiqingHuang ChongbiaoChang AntaoHao Jihui - Osteosarcoma (OS) is a highly aggressive bone cancer with complex molecular mechanisms and variable patient outcomes. This study delineates the paraptosis-related genes (PRGs) landscape in OS and its association with prognosis and the immune microenvironment using bioinformatics approaches. Sixty PRGs were identified and annotated in the Therapeutically Applicable Research to Generate Effective Treatments (TARGET) and GSE21257 cohorts. Consensus clustering stratified patients into molecular clusters, revealing significant survival differences. A risk score was developed using LASSO-Cox regression, which effectively stratified patients into high and low-risk groups. Immune profiling revealed significant differences in immune cell infiltration, with high-risk groups exhibiting decreased levels of activated immune cells. Pathway enrichment analysis indicated higher activity in WNT/BETA-CATENIN, TGF-BETA, and KRAS signaling pathways in high-risk groups. Single-cell RNA sequencing highlighted elevated TNK2 expression in malignant cells. Functional assays confirmed TNK2's role in cell proliferation, viability, and migration, and showed that TNK2 knockdown mitigated cycloheximide-induced proliferation inhibition, linking TNK2 to paraptosis regulation. These findings identify key PRGs and their prognostic significance in OS, revealing distinct immune microenvironments and signaling pathways between molecular clusters. This study also underscores the importance of TNK2 in OS pathogenesis and its potential utility in developing personalized treatment strategies. - Source: PubMed
Publication date: 2025/10/28
Zhou LeiTang YongChen ChangweiJiang Jihong - Tyrosine kinase non-receptor2 (TNK2) is a host protein involved in vesicular trafficking, cell spreading, migration, survival, and proliferation. TNK2 has been identified as a conserved host factor for the entry of several non-enveloped RNA viruses, such as Orsay virus in Caenorhabditis elegans and multiple picornaviruses in cells and mice. Although TNK2 was reported as required for influenza A virus infection in a genome-wide CRISPR screen, its role remains contentious as it was not identified in other screens. In this study, we comprehensively evaluated TNK2's function in IAV infection using in vitro and in vivo models. RNAi knockdown and CRISPR knockout of TNK2 in multiple cells showed no significant reduction in IAV infection. Similarly, primary lung fibroblasts and bone marrow-derived macrophages from Tnk2 mice exhibited comparable infection to those from Tnk2 mice. Moreover, Tnk2 mice exhibited no differences in weight loss, survival, lung pathology, or viral load compared to those of Tnk2 mice after IAV infection. Furthermore, the expression of interferon-β and interferon-stimulated genes were not significantly altered in Tnk2 mice compared to that of Tnk2 mice. Together, these results indicate that TNK2 is not a dominant host factor for IAV infection, suggesting it may not be a viable therapeutic target. - Source: PubMed
Liu SisiFang YiqunLi LingyuHuo JingwenLiu BinyiWang JianhaoXu JiminSong FangzhouLi HaiyuJiang Hongbing