13 results match your criteria ptprj promotes

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PTPRJ promotes osteoclast maturation and activity by inhibiting Cbl-mediated ubiquitination of NFATc1 in late osteoclastogenesis.

FEBS J 2021 08 5;288(15):4702-4723. Epub 2021 Mar 5.

Department of Molecular Genetics, The Weizmann Institute of Science, Rehovot, Israel.

Bone-resorbing osteoclasts (OCLs) are multinucleated phagocytes, whose central roles in regulating bone formation and homeostasis are critical for normal health and development. OCLs are produced from precursor monocytes in a multistage process that includes initial differentiation, cell-cell fusion, and subsequent functional and morphological maturation; the molecular regulation of osteoclastogenesis is not fully understood. Here, we identify the receptor-type protein tyrosine phosphatase PTPRJ as an essential regulator specifically of OCL maturation. Read More

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Disrupting the transmembrane domain-mediated oligomerization of protein tyrosine phosphatase receptor J inhibits EGFR-driven cancer cell phenotypes.

J Biol Chem 2019 12 1;294(49):18796-18806. Epub 2019 Nov 1.

Department of Chemistry, Lehigh University, Bethlehem, Pennsylvania 18015. Electronic address:

Receptor protein tyrosine phosphatases (RPTPs) play critical regulatory roles in mammalian signal transduction. However, the structural basis for the regulation of their catalytic activity is not fully understood, and RPTPs are generally not therapeutically targetable. This knowledge gap is partially due to the lack of known natural ligands or selective agonists of RPTPs. Read More

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December 2019

Loss of DEP-1 (Ptprj) promotes myeloproliferative disease in -ITD acute myeloid leukemia.

Haematologica 2018 11 7;103(11):e505-e509. Epub 2018 Jun 7.

Institute of Molecular Cell Biology, Center for Molecular Biomedicine (CMB), Jena University Hospital

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November 2018

Ptprj-as1 mediates inflammatory injury after intracerebral hemorrhage by activating NF-κB pathway.

Eur Rev Med Pharmacol Sci 2018 05;22(9):2817-2823

Department of Neurosurgery, the First Affiliated Hospital of Jinan University, Guangzhou, China.

Objective: We aimed at investigating the expression of long non-coding RNA (lncRNA) Ptprj-as1 and the role of lncRNAPtprj-as1 in inflammatory cells after intracerebral hemorrhage and its potential mechanism.

Materials And Methods: The rat model of intracerebral hemorrhage was established. Expressions of Ptprj-as1 and inflammatory cytokines in inflammatory cells were detected by quantitative Real-time PCR (qRT-PCR). Read More

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The protein-tyrosine phosphatase DEP-1 promotes migration and phagocytic activity of microglial cells in part through negative regulation of fyn tyrosine kinase.

Glia 2017 02 17;65(2):416-428. Epub 2016 Nov 17.

Institute of Molecular Cell Biology, Center for Molecular Biomedicine (CMB), Jena University Hospital, Hans-Knöll-Straße 2, Jena, Germany.

Microglia cells are brain macrophages whose proper functioning is essential for maintenance and repair processes of the central nervous system (CNS). Migration and phagocytosis are critical aspects of microglial activity. By using genetically modified cell lines and knockout mice we demonstrate here that the receptor protein-tyrosine phosphatase (PTP) DEP-1 (also known as PTPRJ or CD148) acts as a positive regulator of both processes in vitro and in vivo. Read More

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February 2017

The protein tyrosine phosphatase DEP-1/PTPRJ promotes breast cancer cell invasion and metastasis.

Oncogene 2015 Oct 16;34(44):5536-47. Epub 2015 Mar 16.

CRCHUM - Centre de recherche du Centre Hospitalier de l'Université de Montréal, Institut du Cancer de Montréal, Montréal, QC, Canada.

DEP-1/PTPRJ is a receptor-like protein tyrosine phosphatase mainly known for its antiproliferative and tumor-suppressive functions. Many identified substrates are growth factor receptors, and DEP-1 is deleted and/or mutated in human cancers including that of the breast. However, DEP-1 was also identified as a promoter of Src activation and proinvasive functions in the endothelium, suggesting it could perhaps mediate breast cancer invasiveness that is likewise driven by Src family kinases. Read More

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October 2015

Deficiency of the protein-tyrosine phosphatase DEP-1/PTPRJ promotes matrix metalloproteinase-9 expression in meningioma cells.

J Neurooncol 2015 May 12;122(3):451-9. Epub 2015 Feb 12.

Institute of Molecular Cell Biology, CMB, Jena University Hospital, Hans-Knöll-Strasse 2, 07745, Jena, Germany.

Brain-invasive growth of a subset of meningiomas is associated with less favorable prognosis. The molecular mechanisms causing invasiveness are only partially understood, however, the expression of matrix metalloproteinases (MMPs) has been identified as a contributing factor. We have previously found that loss of density enhanced phosphatase-1 (DEP-1, also designated PTPRJ), a transmembrane protein-tyrosine phosphatase, promotes meningioma cell motility and invasive growth in an orthotopic xenotransplantation model. Read More

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Blockage of PTPRJ promotes cell growth and resistance to 5-FU through activation of JAK1/STAT3 in the cervical carcinoma cell line C33A.

Oncol Rep 2015 Apr 29;33(4):1737-44. Epub 2015 Jan 29.

Department of Radiotherapy Oncology, Gansu Provincial Hospital, Lanzhou 730000, P.R. China.

Gene therapy is a promising therapeutic approach for chemoresistant cervical cancers. Therapeutic interventions targeting the key factors contributing to the initiation and progression of cervical cancer may be a more effective treatment strategy. In the present study, we firstly determined the expression of protein tyrosine phosphatase receptor J (PTPRJ) in 8-paired human cervical tumor and non-tumor tissues. Read More

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CD148 tyrosine phosphatase promotes cadherin cell adhesion.

PLoS One 2014 11;9(11):e112753. Epub 2014 Nov 11.

Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN, United States of America; Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN, United States of America.

CD148 is a transmembrane tyrosine phosphatase that is expressed at cell junctions. Recent studies have shown that CD148 associates with the cadherin/catenin complex and p120 catenin (p120) may serve as a substrate. However, the role of CD148 in cadherin cell-cell adhesion remains unknown. Read More

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Phosphorylation of DEP-1/PTPRJ on threonine 1318 regulates Src activation and endothelial cell permeability induced by vascular endothelial growth factor.

Cell Signal 2014 Jun 28;26(6):1283-93. Epub 2014 Feb 28.

CRCHUM - Centre de recherche du Centre Hospitalier de l'Université de Montréal and Institut du Cancer de Montréal, Montréal, Québec, Canada; Department of Medicine, Université de Montréal, Montréal, Québec, Canada. Electronic address:

The protein tyrosine phosphatase DEP-1/PTPRJ positively regulates Src family kinases and critical biological functions in endothelial and hematopoietic cells. Phosphorylation of DEP-1 on Y1311/Y1320 mediates the association and activation of Src, and promotes Src-dependent angiogenic responses including endothelial cell permeability. We have identified T1318 as a phosphorylated residue proximal to Y1320. Read More

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The phosphatase CD148 promotes airway hyperresponsiveness through SRC family kinases.

J Clin Invest 2013 May 1;123(5):2037-48. Epub 2013 Apr 1.

Division of Rheumatology and Rosalind Russell Medical Research Center for Arthritis, University of California San Francisco (UCSF), San Francisco, California, USA.

Increased airway smooth muscle (ASM) contractility and the development of airway hyperresponsiveness (AHR) are cardinal features of asthma, but the signaling pathways that promote these changes are poorly understood. Tyrosine phosphorylation is tightly regulated by the opposing actions of protein tyrosine kinases and phosphatases, but little is known about whether tyrosine phosphatases influence AHR. Here, we demonstrate that genetic inactivation of receptor-like protein tyrosine phosphatase J (Ptprj), which encodes CD148, protected mice from the development of increased AHR in two different asthma models. Read More

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The tyrosine kinase c-Met contributes to the pro-tumorigenic function of the p38 kinase in human bile duct cholangiocarcinoma cells.

J Biol Chem 2012 Nov 28;287(47):39812-23. Epub 2012 Sep 28.

International Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute, Second Military Medical University, Shanghai 200438.

Pro-tumorigenic function of the p38 kinase plays a critical role in human cholangiocarcinogenesis. However, the underlying mechanism remains incompletely understood. Here, we report that c-Met, the tyrosine kinase receptor for hepatocyte growth factor (HGF), contributes to the pro-tumorigenic ability of p38 in human cholangiocarcinoma cells. Read More

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November 2012

Tyrosine phosphorylation of DEP-1/CD148 as a mechanism controlling Src kinase activation, endothelial cell permeability, invasion, and capillary formation.

Blood 2012 Sep 16;120(13):2745-56. Epub 2012 Aug 16.

Centre de recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM) and Institut du Cancer de Montréal, Montréal, QC, Canada.

DEP-1/CD148 is a receptor-like protein tyrosine phosphatase with antiproliferative and tumor-suppressive functions. Interestingly, it also positively regulates Src family kinases in hematopoietic and endothelial cells, where we showed it promotes VE-cadherin-associated Src activation and endothelial cell survival upon VEGF stimulation. However, the molecular mechanism involved and its biologic functions in endothelial cells remain ill-defined. Read More

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September 2012
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