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Human Monoclonal PTPRJ Primary Antibody for CyTOF, FACS - ABIN4900751
Cabezón, Sintes, Llinàs, Benitez-Ribas: Analysis of HLDA9 mAbs on plasmacytoid dendritic cells. in Immunology letters 2010
Show all 5 Pubmed References
Human Monoclonal PTPRJ Primary Antibody for FACS - ABIN4898524
Llinàs, Lázaro, de Salort, Matesanz-Isabel, Sintes, Engel: Expression profiles of novel cell surface molecules on B-cell subsets and plasma cells as analyzed by flow cytometry. in Immunology letters 2010
Show all 2 Pubmed References
Human Monoclonal PTPRJ Primary Antibody for FACS - ABIN4898523
Rollin, Pouplard, Gratacap, Leroux, May, Aupart, Gouilleux-Gruart, Payrastre, Gruel: Polymorphisms of protein tyrosine phosphatase CD148 influence FcγRIIA-dependent platelet activation and the risk of heparin-induced thrombocytopenia. in Blood 2012
Arg326Gln polymorphism is associated with colorectal cancer.
PTPRJ variant of uncertain significance in candidate gene was identified in Familial Mitral Valve Prolapse.
Short variant of the receptor protein phosphatase PTPRJ generated by an alternative splicing promotes angiogenesis in HUVEC cells and tumor angiogenesis.
study reveals the crucial role of miR-155/PTPRJ/AKT axis in proliferation and migration of colorectal cancer cells and suggests a therapeutic potential of PTPRJ.
Authors demonstrate that mtp53 prevents the COP1/DET1 complex from ubiquitinating ETS2 and thereby marking it for destruction. Authors show that mtp53 destabilizes DET1 and also disrupts the DET1/ETS2 complex thereby preventing ETS2 degradation.
These data support that PTPN22 1858C/T, PTPRJ 2965C/G and 1176 A/C polymorphisms and ACP1 A, B and C alleles are not associated with a higher risk of immune thrombocytopenia P in adults.
Loss of PTPRJ expression may predict an aggressive clinical course in ESCC patients.
The strongest association with frailty was observed in the Protein Tyrosine Phosphatase, Receptor type, J (PTPRJ) (rs1566729, P = 0.001372, beta = 0.09397) gene.
the combination of CD200 and CD148 may have a potential differential diagnostic value in leukemic B-CLPDs, especially between CLL and MCL.
These results demonstrated Ptprj as a physiological enzyme that attenuates insulin signalling in vivo, and indicate that an inhibitor of Ptprj may be an insulin-sensitizing agent.
CD148 tyrosine phosphatase promotes e-cadherin cell adhesion.
The studies suggest induction of MMP-9 expression promoted by DEP-1 deficiency.
Moderate expression of DEP-1 was associated with the increased relapse.
C33A cells lacking PTPRJ had increased cell viability, growth, migration, G1-S transition, and 5-FU resistance. PTPRJ negatively regulated the JAK1/STAT3 pathway by decreasing phosphorylation levels of JAK1 and STAT3 and expression of downstream factors.
The expression profiles of DEP1 and B2MG correlate with increased cell senescence and survival in breast cancer.
Phosphorylation of T1318 is part of a regulatory mechanism that channels the activity of DEP-1 towards Src to allow its optimal activation and the promotion of endothelial cell permeability.
Data indicate that CD148 is upregulated in macrophages and T cells in rheumatoid arthritis (RA) samples, and its activity is enhanced by treatment with tumour necrosis factor alpha (TNFalpha), and reduced by synovial fluid or oxidising conditions.
our data support the notion of DEP-1 as positive functional regulator in vascular cerebral arteriogenesis, involving differential PDGF-B gene expression.
FLT3 is a bona fide substrate of DEP-1 and that interaction occurs mainly via an enzyme-substrate complex formation triggered by FLT3 ligand stimulation.
haplotypes in PTPRJ gene may play a role in susceptibility to Non-Hodgkin's lymphoma, by affecting activation of PTPRJ in these B-cell lymphomas.
This study establishes Csk and CD148 as critical molecular switches controlling the thrombotic and hemostatic capacity of platelets and reveals cell-intrinsic mechanisms that prevent pathological thrombosis from occurring.
This study demonstrated that the protein-tyrosine phosphatase DEP-1 promotes migration and phagocytic activity of microglial cells in part through negative regulation of fyn tyrosine kinase.
our results established DEP-1 as an essential driver of VEGF-dependent permeability, angiogenesis, and metastasis
DEP-1 acts as an endogenous antagonist of the insulin receptor, and downregulation of DEP-1 results in an improvement of insulin sensitivity.
Data indicate that CD148 mRNA is upregulated in diseased joints of with collagen-induced arthritis.
The large ectodomains of CD45 and CD148 modulate their inhibitory effect by enabling their passive, size-based segregation from ligated TCR, supporting the kinetic-segregation model of TCR triggering.
phosphatase CD148 promotes airway hyperresponsiveness through SRC family kinases
These data indicate that PTPRJ may regulate differentiation of normal mammary epithelia and that dysregulation of protein localisation may be associated with tumorigenesis.
CD148 plays a dominant role in activating Src family kinases in platelets relative to PTP-1B. Both PTPs are required for optimal platelet activation and aggregate formation under high arterial shear rates.
CD45 and CD148 preferentially target different SFK members (Hck and Fgr versus Lyn, respectively) to positively and negatively regulate GPCR pathways.
differential effects of CD148 in T cells and other leukocyte subsets
DEP-1 is negatively regulating FLT3 signaling activity and that its loss may contribute to but is not sufficient for leukemogenic cell transformation.
CD148 plays a critical role in regulating GPVI/FcR gamma-chain expression and maintains a pool of active SFKs in platelets by directly dephosphorylating the C-terminal inhibitory tyrosines of SFKs that is essential for platelet activation
This protein is a candidate for the mouse colon cancer susceptibility locus (Scc1).
CD148 has a role in developmental vascular organization and regulates endothelial proliferation and endothelium-pericyte interactions
participates in contact inhibition of VEGF signaling
negative regulation of growth-factor stimulated cell migration and promotion of cell-matrix adhesion may be related to the function of DEP-1 as tumor suppressor
Analysis of CD148 and CD45 doubly deficient B cells and macrophages revealed hyperphosphorylation of C-terminal inhibitory tyrosine of SFKs accompanied by substantial alterations in B and myeloid lineage development and defective immunoreceptor signaling
CD148 is a global regulator of platelet activation and a novel antithrombotic drug target.
The protein encoded by this gene is a member of the protein tyrosine phosphatase (PTP) family. PTPs are known to be signaling molecules that regulate a variety of cellular processes, including cell growth, differentiation, mitotic cycle, and oncogenic transformation. This PTP possesses an extracellular region containing five fibronectin type III repeats, a single transmembrane region, and a single intracytoplasmic catalytic domain, and thus represents a receptor-type PTP. This protein is present in all hematopoietic lineages, and was shown to negatively regulate T cell receptor signaling possibly through interfering with the phosphorylation of Phospholipase C Gamma 1 and Linker for Activation of T Cells. This protein can also dephosphorylate the PDGF beta receptor, and may be involved in UV-induced signal transduction. Multiple transcript variants encoding different isoforms have been found for this gene.
receptor-type tyrosine-protein phosphatase eta
, density enhanced phosphatase-1
, protein tyrosine phosphatase, receptor type, J
, receptor-type tyrosine-protein phosphatase eta-like
, CD148 antigen
, HPTP eta
, density-enhanced phosphatase 1
, human density enhanced phosphatase-1
, protein tyrosine phosphatase, receptor type, J polypeptide
, protein-tyrosine phosphatase eta
, protein-tyrosine phosphatase receptor type J
, susceptibility to colon cancer 1, mouse, homolog of
, HPTP beta-like tyrosine phosphatase
, colon tumor susceptibility 1
, susceptibility to colon cancer 1
, supporting-cell antigen