PTPRK Antibody
- Known as:
- PTPRK Antibody
- Catalog number:
- XW-8159
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- PTPRK Antibody
Related genes to: PTPRK Antibody
- Gene:
- PTPRK NIH gene
- Name:
- protein tyrosine phosphatase receptor type K
- Previous symbol:
- -
- Synonyms:
- R-PTP-kappa
- Chromosome:
- 6q22.33
- Locus Type:
- gene with protein product
- Date approved:
- 1998-02-09
- Date modifiied:
- 2019-02-14
Related products to: PTPRK Antibody
Related articles to: PTPRK Antibody
- Protein tyrosine phosphatase kappa (PTPRK), a recognized tumor suppressor, has been implicated in cancer progression of certain solid tumors. This study investigated the role of PTPRK in the progression of pancreatic cancer. - Source: PubMed
Publication date: 2026/05/01
Fang ZiqianLiu XiangyiTian XiuyunAl-Sarireh BilalHao ChunyiJiang Wen GYe Lin - Extranodal natural killer/T-cell lymphoma (ENKTL) is clinically characterized by destructive lesions that first appear in the nasal cavity and progress along the midline of the face. It was historically described as "rhinitis gangrenosa progressiva" or "lethal midline granuloma" due to its destructive clinical nature and had significant diagnostic and therapeutic challenges. This review synthesizes about 40 years of research, beginning with the 1980s and 1990s, when the disease was identified as a T-cell- or NK-cell-derived lymphoma, and the authors' discovery that clearly linked it to Epstein-Barr virus (EBV). ENKTL is highly prevalent in East Asia and characterized by a type II EBV latency pattern, in which the oncoprotein latent membrane protein 1 (LMP1) acts as a central driver of pathogenesis, activating critical signaling pathways including JAK/STAT, NF-κB, PI3K/Akt, and RAS/MAPK. These pathways, often bolstered by mutations in genes, trigger an oncogenic cascade involving epigenetic modifiers-enhancer of zeste homolog 2 (EZH2), histone deacetylase (HDAC). The deletion of chromosome 6q, leading to loss of function of tumor suppressor PR domain zinc finger protein 1 (PRDM1) and forkhead box O3 (FOXO3), as well as transcription of TNF α-induced protein 3 (TNFAIP3) and protein tyrosine phosphatase receptor type kappa (PTPRK), also contributes to pathogenesis. In vitro studies by the author's group demonstrated that autocrine/paracrine positive feedback loops involving several pro-proliferative molecules/cytokine/chemokine-CD27, ICAM1, hepatocyte growth factor (HGF), IL-9, IL-10, IL-15, CCL17, CCL22, CXCL10- further amplify ENKTL proliferation. Diagnostic precision has improved through the use of serum EBV DNA copy numbers and viral microRNAs (miRs), specifically miR-BART2-5p, alongside the emergence of soluble CD27 as a novel biomarker. While early anthracycline-based regimens failed due to multidrug resistance (MDR), modern concurrent chemoradiotherapy composed of MDR-independent drugs has significantly improved 5-year overall survival (OS) rates for localized disease to over 80%. For advanced or relapsed/refractory cases, L-asparaginase-based regimens are standard, though outcomes remain unsatisfactory. The therapeutic paradigm is currently shifting toward chemoradiotherapy combined with either immune checkpoint inhibitors or small-molecule drugs. Future research should focus on novel molecular-targeted therapies, immunotherapies, or combination strategies targeting proliferation-related molecules or LMP1. - Source: PubMed
Publication date: 2026/04/17
Harabuchi Yasuaki - Gliomas comprise a heterogeneous group of central nervous system tumors in which gene fusions (GFs) are significant oncogenic drivers and emerging diagnostic and therapeutic biomarkers. In cancer diagnosis, GF detection largely relies on targeted short-read sequencing fusion panels, such as the Children's Hospital of Philadelphia (CHOP) Fusion Panel (FUSIP). While these panels are effective for detecting recurrent, well-characterized GFs, they are limited to predefined gene sets and cannot identify full-length transcripts. Here, we analyzed 49 high- and low-grade gliomas previously classified as fusion-negative by FUSIP using an untargeted whole-transcriptome RNA sequencing approach with Oxford Nanopore Technologies (ONT) long-read sequencing. This enabled transcriptome-wide fusion discovery of additional known and potentially novel oncogenic GFs beyond panel constraints. Long-read sequencing further allowed direct resolution of full-length fusion transcripts and their associated isoform structures. By integrating GF detection with isoform-level transcript analysis, we identified fusion-associated transcript isoforms with alternative splicing patterns that aligned near reported GF breakpoints, including :: and ::, which have not been reported in literature or existing fusion databases. To assess functional relevance, candidate GFs were evaluated using the model, with ventral nerve cord (VNC) morphology serving as a quantitative readout of fusion-induced disruption of glial regulation. VNC enlargement or elongation reflects abnormal glial growth or defects in brain tissue organization. Of the 15 candidate GFs subjected to experimental functional testing, 8 induced significant VNC abnormalities relative to wild-type controls, indicating fusion-specific disruption and oncogenic potential. Notably, :: and :: produced the most pronounced VNC phenotypes. Together, these findings demonstrate that untargeted transcriptome-wide GF discovery, coupled with long-read isoform-level analysis and functional validation, enables the identification and prioritization of potentially novel and clinically relevant GFs that are missed by standard targeted short-read fusion panels in glioma. - Source: PubMed
Publication date: 2026/03/17
Rybacki KarleenaCha Emily Na YoungDeutsch Hannah MGaudet EloiseAhsan Mian UmairXu FengChan JoeLi MarilynSong YuanquanWang Kai - Genetic and epigenetic alterations in colorectal cancer (CRC) have been extensively investigated. Small depressed-type colorectal tumors (DCs) constitute a highly invasive CRC subtype. We characterized the mutational profiles of 22 DC samples, seven of which were subjected to whole exome sequencing (WES). This revealed frequent mutations (7 of 22 cases, 31.8%) in PTPRK, with most of these mutations located in the D1 domain-encoding region. To further quantify the incidence of PTPRK mutations, we analyzed 567 CRCs cases from two public databases (The Cancer Genome Atlas and the Catalogue of Somatic Mutations in Cancer). Mutations were more frequently observed in proximal colon tumors and were highly associated with the CpG island methylator phenotype-positive (CIMP-P) subtype (76.2%) and microsatellite instability (MSI; 66.7%). PTPRK mutant proteins (particularly those with D1 domain) retained the ability to bind integrin beta-4 (ITGB4). In addition, CRC cells expressing PTPRK mutants exhibited increased ITGB4 phosphorylation, suggesting that the mutations impair the phosphatase activity of PTPRK. Consistent with this, tumors with PTPRK mutations proliferated significantly more rapidly than their wild type counterparts in vivo. These findings suggest that PTPRK mutations contribute to DC development by dysregulating phosphorylation-mediated signaling pathways. - Source: PubMed
Publication date: 2026/03/12
Tojo MasayukiShinjo KeikoOhka FumiharuKatsushima KeisukeHatanaka AkiraIchimura NorihisaSuzuki HiromuNozawa HisakoYoshida HitoshiKonishi KazuoKondo Yutaka - This study aimed to identify novel mutations associated with the progression of gastric cancer by establishing patient-derived xenograft (PDX) models and performing comprehensive genomic characterization of these PDX models and their corresponding primary tumors. - Source: PubMed
Publication date: 2026/01/29
Kong LukeWang JieZheng JunqiYang XihuaSun RuifangKou JiahuiYao YujieLi FengWang FuhuaGuo Sutang