Ask about this productRelated genes to: PTK6 antibody
- Gene:
- PTK6 NIH gene
- Name:
- protein tyrosine kinase 6
- Previous symbol:
- -
- Synonyms:
- BRK
- Chromosome:
- 20q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1992-10-02
- Date modifiied:
- 2016-10-05
Related products to: PTK6 antibody
Related articles to: PTK6 antibody
- Pancreatic ductal adenocarcinoma (PDAC) is a malignant tumor associated with poor prognosis and high mortality. The distinct metabolic reprogramming of nutrients in PDAC fosters an immunosuppressive tumor immune microenvironment (TIME) and compromises the efficacy of immunotherapy. Protein tyrosine kinase 6 (PTK6) is highly expressed in multiple solid tumors and contains a short N-terminal region featuring an SH2 domain capable of lipid binding, suggesting its involvement in lipid metabolic reprogramming within the malignant tumor microenvironment. Using PTK6-knockout mouse models and lipidomic sequencing, we investigated how PTK6 drives metabolic dysregulation and immune effector exhaustion in pancreatic tumors. Our findings uncover a "dual driver" role for PTK6 in PDAC progression: While it enhances cancer cell resistance to ferroptosis by the reprogramming lipid metabolism, it also promotes CD8 T cell exhaustion through upregulating PD-1 and Tim-3 expression, ultimately driving immunosuppression. In summary, these findings identify PTK6 as a potential biomarker in PDAC and reveal a previously unrecognized role of PTK6 in linking tumor lipid metabolism to CD8 T cell exhaustion. These data suggest that PTK6 may represent a candidate mechanistic target for further therapeutic exploration. - Source: PubMed
Publication date: 2026/04/28
Zheng RuiWang SiLi DanTian XingSun LifengWang JiaoWang YuchangPan XuyiLiang YifanYang Zhihang - Pancreatic adenocarcinoma (PAAD) is a highly lethal malignancy characterized by a dismal prognosis and limited treatment options. Protein tyrosine kinase 6 (PTK6) is abnormally activated in multiple cancer types. Understanding the function of PTK6 in pancreatic cancer could reveal novel therapeutic targets and prognostic markers. - Source: PubMed
Publication date: 2026/04/28
Wang Feng-JiaoYu Shu-LinYang Pei-WenJiao Ju-YingHou Feng-GangFan Yue - - Source: PubMed
Publication date: 2026/04/24
Zhen ShijunZhu QingtaoWu XinzeXiong FangtaoMa WentaoWang ZishuoBo Wei - Triple-negative breast cancer (TNBC) is an aggressive malignancy lacking effective targeted therapies, underscoring the need for robust and interpretable biomarkers for personalized treatment. Here, we propose a graph attention network (GAT)-based multimodal framework that integrates scRNA-seq, scATAC-seq, and radiomics to capture cross-modal regulatory interactions underlying TNBC heterogeneity. Transcriptional, chromatin accessibility, and imaging features are aligned via canonical correlation analysis, with intercellular communication-derived gene relationships and transcription factor-binding-guided edges incorporated into a multimodal graph. Multi-head attention enables adaptive weighting of omics-specific interactions, while an ensemble multilayer perceptron with variational dropout stratifies patient prognosis. The model demonstrates strong predictive performance in an external TCGA-TNBC cohort (log-rank p<0.01), outperforming single-omics and alternative graph-based approaches (AUC-ROC = 0.839, 95% CI: 0.81-0.87). Pathway analysis validates canonical TNBC drivers, including PI3K, ERBB2, PTK6, and EGFR signaling, while revealing previously underappreciated regulatory programs involving complement-coagulation cascades, ECM-integrin-focal adhesion signaling, leukocyte transendothelial migration, sphingolipid-mediated metabolic-immune coupling, and nanoparticle-receptor interactions. Collectively, this framework provides an interpretable strategy for multimodal biomarker discovery in TNBC, uncovering both established and novel therapeutic vulnerabilities and offering a scalable approach toward precision oncology. - Source: PubMed
Publication date: 2026/04/09
Jiang ZixiCao KexinGe FangHuang Zhusheng - Chromosomal instability (CIN), impaired telomere biology, and aberrant DNA methylation are implicated in colorectal cancer (CRC) development. Tracking these alterations from precancerous lesions through tumors to metastases may reveal biomarkers of CRC initiation and progression. Tissue samples from 44 patients with either high-grade colorectal dysplasia (HGA; n = 13) or advanced metastatic CRC (n = 31) were analyzed. CIN was assessed in all patients using either low-coverage whole-exome sequencing or microarray-based comparative genomic hybridization. In a subset of patients, genome-wide CpG methylation profiling (n = 19) and telomere length measurements (n = 15) were performed. CIN was detected in 85% of HGA patients, spanning focal CNVs in MALAT1 (46%) to recurrent alterations on chromosomes 11, 13, and 20, with PTK6 being the most frequently amplified (61%). CIN was comparable between primary tumors and synchronous metastases but was significantly elevated in metachronous cases. DEK was amplified in all metastases but the aberration was absent in primaries, irrespective of tissue chronicity. Methylation profiling distinguished HGA from adjacent non-dysplastic mucosa (9859 differentially methylated CpGs) and unrelated tumor tissues (17 638 CpGs), whereas primary tumors and metastases differed at only five CpG sites. Both primary tumors and metastases appeared epigenetically younger than colonic mucosa. Metastases exhibited significantly shorter telomeres than both primary tumors (P = .019) and colonic mucosa (P = .001). The amplification of PTK6 may serve as an early biomarker detectable at the HGA stage, while DEK amplification appears crucial for metastatic progression and may represent a therapeutic target. Further validation is needed. - Source: PubMed
Saskova KaterinaLandfors MattiasHlavac ViktorSeborova KarolinaBruha JanHonkova KaterinaTomasova KristynaSelvi SabaDrabova JanaHackenhaar Fernanda SNilsson Torbjörn KVodicka PavelValickova AnnaLiska VaclavFarkas Sanja ADegerman SofieKroupa Michal