PTPRJ Antibody
- Known as:
- PTPRJ Antibody
- Catalog number:
- XW-7821
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- PTPRJ Antibody
Related genes to: PTPRJ Antibody
- Gene:
- PTPRJ NIH gene
- Name:
- protein tyrosine phosphatase receptor type J
- Previous symbol:
- -
- Synonyms:
- DEP1, HPTPeta, CD148
- Chromosome:
- 11p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-09-14
- Date modifiied:
- 2019-02-14
Related products to: PTPRJ Antibody
Related articles to: PTPRJ Antibody
- The liver has a unique capacity for self-renewal, maintaining a proper liver-to-bodyweight ratio, which is essential for sustaining homeostasis. Regenerative process in the liver involves intricate communication between various cell types such as hepatocytes, hepatic stellate cells, endothelial cells, and inflammatory cells. Although the role of endothelial cells in liver regeneration has been extensively studied, detailed knowledge regarding specific endothelial cell-derived factors that promote the regeneration of liver endothelial cells (LECs) remains limited. This study aimed to identify the regenerative capacity of endothelial progenitor cells (EPCs) after acute liver injury. - Source: PubMed
Publication date: 2026/03/28
Lee Jong-MinHa Yoon-SuLee Seung-JunKim Hyun-YiAdpaikar Anish AshokKim Eun-JungOtsu KeishiChe XiangguoHan Dai HoonHer YoungChoi Je-YongKim Seung-JinJung Han-Sung - This study aimed to prioritize candidate transcriptomic mediators associated with human atherosclerosis progression by integrating transformer-based deep learning with classical bioinformatics and experimental validation. Gene expression profiles from dataset GSE100927 (69 plaques, 35 controls) were normalized and analyzed for differential expression using the limma package (FDR < 0.01). A TabTransformer model employing multi-head self-attention was trained (80/20 split, 10-fold cross-validation) to predict disease status, and SHapley Additive exPlanations (SHAP) analysis quantified gene-level contributions. Network topology was examined using STRING and Cytoscape to identify hub genes through betweenness centrality, while pathway enrichment was assessed via GO and KEGG analyses. Among 638 differentially expressed genes (402 upregulated, 236 downregulated), the TabTransformer achieved a mean AUC of 0.964, surpassing the LASSO baseline by 3.8%. The top-ranked genes, TYROBP, TNF, PTPRJ, DHRS9, and COL1A1, were primarily involved in leukocyte activation, NF-κB signaling, and smooth muscle dysfunction. Experimental assays in oxidized LDL-treated human umbilical vein endothelial cells confirmed significant upregulation of TYROBP (6.3-fold) and TNF (4.8-fold), validating computational predictions. These findings support an immunoinflammatory axis linked to the suppression of smooth muscle identity in atherosclerosis, and highlight TYROBP and TNF as mechanistically plausible candidate biomarkers and potential therapeutic targets. - Source: PubMed
Yan DongdongLi WenqiangXing ErkunWang PeiZhang Zheng - Receptor protein tyrosine phosphatases (RPTPs) are key regulators of cell signaling. However, their study and therapeutic targeting have been limited by the lack of known natural ligands or selective agonists, as well as an incomplete understanding of their structure-function relationships. Nonetheless, receptor homodimerization has been shown to suppress RPTP catalytic activity by restricting substrate access, offering a promising strategy for examining and modulating their function. Our previous work on PTPRJ, a member of the RPTP family, showed that its transmembrane domain regulates homodimerization, thereby controlling access to receptor tyrosine kinase (RTK) substrates and their phosphorylation levels. We also developed peptides that disrupt this dimerization, thereby inhibiting RTK phosphorylation and reducing cancer cell migration. These peptides were then engineered for selective, pH-sensitive insertion into the acidic tumor microenvironment to enhance efficacy while limiting off-target effects. Yet how broadly PTPRJ activation reshapes the phosphotyrosine landscape and whether those changes yield coherent cellular phenotypes remains unclear. In this study, we employed tyrosine phosphoproteomics, immunoblotting, immunofluorescence, and functional assays to assess the global impact of our lead peptide candidate, Hybrid 7, in A549 lung cancer cells that endogenously express PTPRJ. We find that Hybrid 7 decreases EGFR phosphorylation and selectively reduces phosphorylation across additional RTKs and motility adaptors, producing strong inhibition of EGF-driven migration and reduced proliferation. Hybrid 7 also elevates reactive oxygen species and DNA damage, and enforces CDK1-dependent G2/M arrest, indicating a primarily cytostatic, checkpoint-mediated response. These findings highlight the potential of RPTP-targeting peptides as valuable tools for dissecting RPTP function and as possible therapeutic agents capable of modulating key oncogenic pathways and inhibiting cancer progression. - Source: PubMed
Publication date: 2025/11/17
Rizzo SophieHart William SFetter Rachel LSong BokaiWhite Forest MLazzara Matthew JThévenin Damien - Advances in minimally invasive surgical techniques and precision oncology paradigms have significantly optimized the management of colorectal cancer (CRC). The advent of endoscopic superminimally invasive surgery (ESMIS) has led to comprehensive evaluations of its proteomic impact in patients with CRC. This prospective study utilized Olink plasma proteomic profiling to delineate ESMIS-versus laparoscopic surgery (LS)-associated molecular variations in CRC cohorts, with validation via immunofluorescence (IF), immunohistochemistry (IHC), and Western blotting (WB) methodologies. The results demonstrated that ESMIS significantly attenuated the surgical invasiveness. Calcitonin (CALCA) and platelet-derived growth factor C (PDGFC) emerged as potential biomarkers for invasive damage assessment, while amnionless (AMN), low-density lipoprotein receptor-related protein 1 (LRP1), forkhead box protein O1 (FOXO1), receptor-type tyrosine-protein phosphatase eta (PTPRJ), and fructose-2,6-bisphosphatase TIGAR were identified as novel diagnostic indicators for CRC. IF, IHC, and WB analyses corroborated Olink findings, confirming significantly decreased AMN, LRP1, FOXO1, and PTPRJ expression in malignant cells and tissues. Future investigations of minimally invasive CRC therapies should prioritize cellular proliferation, metabolic reprogramming, stress response, and apoptosis. Collectively, these findings establish a molecular foundation for precision surgery and provide novel insights into the CRC pathophysiology and iatrogenic organ damage mechanisms. - Source: PubMed
Publication date: 2025/10/30
Yan YangMa YizhaoXiao PanWang JingyuanXiao SaiLinghu EnqiangZhao PengyueChen Qianqian - The treatment of Epstein-Barr virus (EBV)-associated malignancies is increasingly recognizing the necessity of personalized medicine strategies to enhance therapeutic outcomes. This research addresses this need by computationally investigating potential peptide inhibitors targeting the latent membrane protein 1 (LMP1), a key oncoprotein in EBV-related cancers. The study specifically focuses on the C-terminal activating region (CTAR) of LMP1, a critical domain for its oncogenic signalling. To identify promising inhibitors, a comprehensive computational methodology was employed, encompassing Unidock virtual screening, PYRX molecular docking, AMBER molecular dynamics simulations, and CPPTRAJ analysis. This integrated approach led to the identification of a Protein Tyrosine Phosphatase Receptor Type J (PTPRJ) agonist peptide derived from the CancerPPD database as a potential inhibitor of EBV LMP1. PTPRJ is a known tumour suppressor involved in regulating cellular proliferation, migration, and angiogenesis. The findings suggest that the identified peptide agonist may exert its inhibitory effect on LMP1 by activating PTPRJ, thereby influencing cancer cell behaviour and the tumour microenvironment. This research presents a significant starting point for the development of novel therapeutic interventions tailored for EBV-related cancers. The application of computational methods underscores a strategic approach to tackle the complexities of personalized medicine in the context of these malignancies. Furthermore, the focus on the LMP1 CTAR region as a therapeutic target highlights the critical role of this viral protein in driving oncogenesis. The integration of diverse computational tools in this study signifies a rigorous and multifaceted strategy for identifying potential drug candidates. - Source: PubMed
Publication date: 2025/10/07
Salam Dayang-Sharyati D ASan Hwang SiawWezen Xavier Chee