PTPN6 pTyr564 antibody Ab
- Known as:
- PTPN6 pTyr564 (anti-) Antibody
- Catalog number:
- 1488113
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- PTPN6 pTyr564 antibody
Related genes to: PTPN6 pTyr564 antibody Ab
- Gene:
- PTPN6 NIH gene
- Name:
- protein tyrosine phosphatase non-receptor type 6
- Previous symbol:
- -
- Synonyms:
- HCP, HCPH, PTP-1C, SHP-1, SHP1
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-12
- Date modifiied:
- 2019-02-14
Related products to: PTPN6 pTyr564 antibody Ab
Related articles to: PTPN6 pTyr564 antibody Ab
- Genetic variants affecting microglia can cause early-onset neurodegeneration or elevate Alzheimer's disease risk. To nominate regulators of relevant signaling pathways, we developed a genome-wide CRISPR screen in primary macrophages focused on survival. We identified Ptpn6, which encodes the inhibitory phosphatase SHP-1, as a crucial regulator for macrophage survival under reduced CSF1R signaling conditions in vitro. Deletion of Ptpn6 from adult microglia in vivo enhanced survival and decreased neuritic dystrophy around amyloid plaques in the TauPS2APP model of Alzheimer's disease. However, deletion also dysregulated homeostasis in normal white matter and exacerbated neurodegeneration in disease. Heterozygous deletion revealed a differential gene-dosage sensitivity for beneficial and detrimental effects, exhibiting reduced neuritic damage near plaques without white-matter harm. Single-cell RNA sequencing uncovered multiple disease-associated microglia (DAM)-like transcriptional states, with Lgals3 microglia emerging alongside neurodegeneration after Ptpn6 deletion. In all, these findings reveal both the protective and latent degenerative potential of microglia held in check by Ptpn6. - Source: PubMed
Publication date: 2026/03/26
Etxeberria AinhoaLee Seung-HyeKuhn Julia ACallow MarinellaNovikova GloriiaFortin Jean-PhilippeChoy Man KinXie LukeImperio JoseVito SteveTsai Ming-ChiLock JaclynTaraborrelli LuciaHaag Simone MChen HonglinGe MonicaNgu HaiForeman OdedStark KimFriedman Brad AHaley BenjaminHansen David VMeilandt William JEaston AmyMartin ScottMurthy AdityaCosta MikeBohlen Christopher J - The Qingjin Pingchuan Formula (QJPC), a multi-herb traditional Chinese medicine prescription, is clinically employed for severe community-acquired pneumonia (SCAP), though its underlying molecular mechanisms remain incompletely understood. - Source: PubMed
Publication date: 2026/03/12
Zhang YifeiYue RushuangZhang LuyaoJi YiShi RongZhou Qianmei - The Src family kinase Lyn is known to be involved in the induction and maintenance of peripheral B cell tolerance; however, mechanistic separation of tolerogenic functions from the role of Lyn in B cell and myeloid cell development and activation is challenging. Here we utilize a system in which Lyn deletion is tamoxifen inducible and B cell restricted, which allows acute elimination of Lyn in B cells only, minimizing confounding factors. This genetic tool is employed in conjunction with immunoglobulin transgenic mice in which peripheral B cells are autoreactive. DNA reactive Ars/A1 B cells require continuous inhibitory signaling, mediated by the inositol phosphatase SHIP-1 and the tyrosine phosphatase SHP-1, to maintain an unresponsive (anergic) state. Here we show that Ars/A1 B cells require Lyn to establish and maintain B cell unresponsiveness via restricting PI3K-dependent signaling pathways. This Lyn-dependent mechanism complements the impact of reduced mIgM B cell receptor (BCR) expression to restrict BCR signaling in Ars/A1 B cells. Our findings thus suggest that a subset of autoreactive B cells requires Lyn to become anergic and that the autoimmunity associated with dysregulated Lyn function may, in part, be due to an inability of these autoreactive B cells to become tolerized. - Source: PubMed
Publication date: 2026/03/08
Fiske Brigita EWemlinger Scott MCrute Bergren WGetahun Andrew - Shp1 is a cytosolic tyrosine phosphatase generally associated with antitumor effects through the inhibition of tyrosine kinase signaling. Herein, we shown that genetic and pharmacological inhibition of Shp1 in breast cancer cells induces accelerated cell migration and promotes a more invasive phenotype. Furthermore, we found that interleukin-8 (IL8), a chemokine with multiple pro-tumorigenic roles within the tumor microenvironment, directly modulates Shp1 activity. In breast cancer, IL8 elicits its functions through the binding to the CXCR2 receptor with the subsequent modulation of several intracellular signaling pathways. We show that in breast MCF7 cells, IL8 induces the PKC-mediated phosphorylation of Shp1 at Ser591, diminishing its enzymatic activity and impairing the dephosphorylation of PP2A; this enhances CXCR2 phosphorylation and alters receptor trafficking by promoting ubiquitination and degradation of CXCR2. This feedback mechanism limits IL8 signaling revealing a previously unrecognized mechanism of receptor turnover and signal attenuation. In addition, we found that Shp1-mediated regulation of CXCR2 directly influences IL8-driven invasiveness in a subtype-specific manner, affecting luminal and triple-negative breast cancer (TNBC) cells but not HER2-positive ones. Transcriptomic and pathway analyses further support Shp1 involvement in cytokine and GPCR signaling, particularly in TNBC, where its downregulation correlates with reduced survival and higher IL8 levels. Taken together, our findings elucidate a novel mechanism of IL8 signaling and identify Shp1 as a promising therapeutic target, highlighting the potential of modulating the CXCR2-Shp1 axis to limit invasiveness and metastasis in aggressive breast cancer subtypes, particularly TNBC. - Source: PubMed
Publication date: 2026/03/02
Monti MarcelloAmendola Pier GiorgioFilograna AngelaGargiulo SabrinaAllegretti MarcelloCorda DanielaVarone Alessia - : The exact pathogenesis of Alzheimer's disease (AD), a neurodegenerative disorder, remains unclear. Ferroptosis is a form of cell death characterized by intracellular iron accumulation, and has emerged as a potential contributor to the pathological cascade of AD. Therefore, this study aims to identify core genes that may function as reliable biomarkers for AD through an in-depth analysis of the genetic relationship between ferroptosis-related genes and AD. : This study first obtained the gene expression profiles (GSE140831, GSE63060 and GSE63061 expression profiles). The GSE140831 dataset served as the discovery cohort, and the GSE63060 and GSE63061 datasets were used as independent validation cohorts. R language 4.4.1 was used for standardizing and identifying differentially expressed genes (DEGs) in AD patients in all datasets. Secondly, the ferroptosis-related genes were obtained. By integrating the ferroptosis-related genes, ferroptosis-related DEGs (FRDEGs) were detected. Then, the FRDEGs were verified and evaluated, and the biological functions of the core genes were analyzed. Finally, miRNAs interacting with these core FRDEGs were explored. : The study identified nine FRDEGs (ACVR1B, BRPF1, G6PD, KLHDC3, LAMP2, MTCH1, P4HB, PTPN6, RBMS1), which are potentially related and may serve as biomarkers for AD. All nine genes demonstrated statistically significant differential expression (up-regulation) in both independent validation cohorts and in the combined analysis ( < 0.05). Although the area under the curve (AUC) values of these nine genes ranged from 0.61 to 0.71, indicating moderate discriminatory power, these findings suggest that they may be involved in pathways related to AD and are worthy of further investigation as potential auxiliary biomarkers. Finally, a network of hub FRDEGs-miRNAs interaction was constructed. There were 11 miRNAs that may regulate these hub FRDEGs simultaneously. : This study showed the significant association of the identified FRDEGs with AD. Also, a core ferroptosis-related biomarker network for miRNAs regulation of AD was constructed. The specific regulatory mechanism is worthy of further investigation. - Source: PubMed
Publication date: 2026/02/11
Liu WenjiaRao XinYu Liyang