Ask about this productRelated genes to: PTP1B protein
- Gene:
- PTPN1 NIH gene
- Name:
- protein tyrosine phosphatase non-receptor type 1
- Previous symbol:
- PTP1B
- Synonyms:
- -
- Chromosome:
- 20q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1991-09-13
- Date modifiied:
- 2019-02-14
Related products to: PTP1B protein
Related articles to: PTP1B protein
- Natural killer (NK) cells are promising candidates for allogeneic anti-cancer immunotherapy. However, their cytolytic activity is often suppressed by the tumor microenvironment. We demonstrate that genetic silencing or pharmacological dual inhibition of protein tyrosine phosphatases PTPN1 and PTPN2 (PTPN1/N2) in NK cells significantly enhances anti-tumor cytolytic activity both in vitro and in vivo. This augmented NK cell activity is mediated by increased expression of early activation markers and the production of effector molecules such as granzyme B and interferon-gamma (IFN-γ). Notably, this elevated cell cytolytic response remains substantially resistant to the immunosuppressive effects of TGFβ-1, a cytokine known to dampen NK cell activity and commonly present in the tumor microenvironment. Mechanistically, targeting PTPN1/N2 in NK cells promotes JAK/STAT signaling pathways and sensitizes cells to IL-2 stimulation. Importantly, dual inhibition of PTPN1/N2 markedly enhances the cytolytic activity of cord blood NK cells against patient-derived glioblastoma cells, highlighting the potential of this approach for future therapeutic applications. These findings provide compelling evidence that dual targeting of PTPN1/N2 could significantly improve the efficacy of therapeutic "off-the-shelf" NK cell-based immunotherapy. - Source: PubMed
Publication date: 2026/04/15
Feng Chu-HanPeltier LindaChouleur TiffanieDiPonzio MileaAubry IsabellePoirier Alexandre JCordova Zuzet MShen YunyunTabariès SébastienCao XiaonaChen GuojunBikfalvi AndreasVidal Silvia MSiegel Peter MLaneuville PierreTremblay Michel L - Excessive macrophage activation is thought to be the primary cause of the cytokine storm that results in severe coronavirus disease 2019 (COVID-19) complications. The underlying mechanisms remain elusive, and more research is needed to find disease-critical genes and develop effective therapies. In this study, we used publicly accessible microarray datasets of cytokine storm in cultured human monocyte-derived macrophages challenged with cytokines, and employed bioinformatics, such as weighted gene co-expression network analysis (WGCNA) and differential expression analysis, to dissect gene expression profiles and identify putative disease-related molecules. Initially, three co-expression modules and related key genes were discovered, which highly correlated to macrophages challenged with cytokines. Then, a preliminary gene expression signature consisting of 203 upregulated and 24 downregulated genes was identified. Next, protein-protein interaction analysis and hub gene identification were used to identify 11 crucial hub genes, namely (), (), (), (), (), (), (), (), (), () and (). Then, the LINCS L1000 characteristic direction signatures search engine (L1000CDS2) was employed for drug repurposing studies. Dasatinib was predicted to be the leading therapeutic compound to perturb the gene signature of cytokine storm in human macrophages. Connectivity Map results suggested that dasatinib may normalize ICAM-1 expression. In addition, the results of molecular docking studies and molecular dynamics simulation revealed that dasatinib may spontaneously interact with ICAM-1 via several key residues and form a relatively stable protein-ligand complex. Overall, this work, based on an analysis of co-expression correlation networks, gene expression signatures and pivotal genes in human macrophages challenged with cytokines, combined with drug repurposing studies, demonstrated that dasatinib may interact with ICAM-1 and could be a potential candidate for cytokine storm. However, due to the limitations of computational approaches, further experimental validation is necessary. - Source: PubMed
Publication date: 2026/03/27
Chen ShaojunWu DapengZheng ZheLuo YiyuanZhang Lihua - Obesity-related adipose tissue dysfunction leads to a chronic inflammatory state affecting distant organs and tissues. This metabolic inflammation has a detrimental impact on the expression of genes related to glucose metabolism, leading to systemic insulin resistance, which also affects the central nervous system and contributes to cognitive decline. Adipose tissue-derived microRNAs (miRNAs) have been implicated in this phenomenon. This study aimed to investigate whether the expression of genes critical for both insulin action and neuronal metabolism (APP, SOCS3, PTPN1, PTPN2) is altered in the adipose tissue of patients with obesity due to miRNA interference, predisposing them directly to the development of insulin resistance and metabolic inflammation, while indirectly leading to a decline in cognitive function. - Source: PubMed
Publication date: 2026/04/13
Podraza JakubWąsowski MichałJonas Marta IzabelaLisik WojciechJonas MaurycyBinda ArturJaworski PawełTarnowski WiesławNoszczyk BartłomiejPuzianowska-Kuźnicka MonikaKuryłowicz Alina - Protein tyrosine phosphatases (PTPs) counteract receptor tyrosine kinase (RTK) signaling. Inhibition of PTPs by oxidation can be reversed by cytosolic thioredoxin (TXN), but less is known about regulation of PTPs by glutathione (GSH)-driven glutaredoxins (GLRXs). Here, we thus assessed GLRX1, GLRX2, and/or TXN1 in regulation of CO/bicarbonate- and HO-mediated oxidation of the physiologically important PTP1B. GLRXs and TXN1 synergistically maintained PTP1B activity, and modulating cellular levels of either GLRX1, GLRX2, or TXN1 gave strong effects on phosphorylation cascades triggered by epidermal growth factor (EGF) or platelet-derived growth factor (PDGF). Furthermore, transient intracellular interactions of PTP1B with GLRX1, GLRX2, and TXN1 were discovered within minutes after stimuli with either PDGF or EGF, coinciding with control of the corresponding RTK-driven phosphorylation cascades. We conclude that TXN1 and GLRXs are key regulators of PTP1B activity and thus control cellular responses to RTK stimulation. - Source: PubMed
Publication date: 2026/04/10
Coppo LuciaZhao WenchaoCheng QingScholz Axel TobiasArnér Elias S JDagnell Markus - Aicardi-Goutières syndrome (AGS) is a type I interferonopathy presently associated with nine genes. is a negative regulator of the interferon pathway previously associated with chronic inflammation and recently type 1 IFN autoinflammation. - Source: PubMed
Publication date: 2026/04/01
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