Anti-PTPRJ monoclonal antibody, clone FQS24409

Name: Anti-PTPRJ monoclonal antibody, clone FQS24409
SKU: DCABH-7222
Rating: 5 (1 reviews)

Rabbit anti-Human PTPRJ monoclonal antibody for WB

COA

SDS

Datasheet

Summary

Specifications

Antibody Isotype

IgG

Clone

FQS24409

Species Reactivity

Mouse; Rat; Human

Immunogen

Synthetic peptide (the amino acid sequence is considered to be commercially sensitive) within Human DEP1 aa 150-250. The exact sequence is proprietary.Database link: Q12913

Conjugate

Unconjugated

Applications

Application Notes

WB: 1/1000 - 1/10000.

Target

Alternative Names

PTPRJ; protein tyrosine phosphatase, receptor type, J; receptor-type tyrosine-protein phosphatase eta; CD148; DEP1; HPTPeta; DEP-1; R-PTP-J; HPTP eta; CD148 antigen; density-enhanced phosphatase 1; protein-tyrosine phosphatase eta; human density enhanced

Entrez Gene ID

5795

UniProt ID

Q12913

Product Background

Antigen Description

Tyrosine phosphatase which dephosphorylates or contributes to the dephosphorylation of CTNND1, PDGFRB, MET, RET (variant MEN2A), KDR, LYN, SRC, MAPK1, MAPK3, EGFR, TJP1, OCLN, PIK3R1 and PIK3R2. Plays a role in cell adhesion, migration, proliferation and differentiation. Involved in vascular development. Regulator of macrophage adhesion and spreading. Positively affects cell-matrix adhesion. Positive regulator of platelet activation and thrombosis. Negative regulator of cell proliferation. Negative regulator of PDGF-stimulated cell migration; through dephosphorylation of PDGFR. Positive regulator of endothelial cell survival, as well as of VEGF-induced SRC and AKT activation; through KDR dephosphorylation. Negative regulator of EGFR signaling pathway; through EGFR dephosphorylation. Enhances the barrier function of epithelial junctions during reassembly. Negatively regulates T-cell receptor (TCR) signaling. Upon T-cell TCR activation, it is up-regulated and excluded from the immunological synapses, while upon T-cell-antigen presenting cells (APC) disengagement, it is no longer excluded and can dephosphorylate PLCG1 and LAT to down-regulate prolongation of signaling.

Pathway

Adherens junction, organism-specific biosystem; Adherens junction, conserved biosystem; PDGFR-beta signaling pathway, organism-specific biosystem; Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met), organism-specific biosystem; T Cell Receptor Signaling Pathway, organism-specific biosystem;

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Loss of the phosphatase PTPRJ causes migration defects of megakaryocytes and thrombocytopenia

EUROPEAN JOURNAL OF HUMAN GENETICS

Authors: Marconi, C.; Faleschini, M.; Palombo, F.; Bottega, R.; Bozzi, V.; Noris, P.; Balduini, A.; Pippucci, T.; Savoia, A.; Balduini, C. L.; Katsanis, N.; Pecci, A.; Seri, M.

Abstract

Genome-wide disease association study in chewing tobacco associated oral cancers

ORAL ONCOLOGY

Authors: Bhatnagar, Renu; Dabholkar, Jyoti; Saranath, Dhananjaya

Abstract

With a view to identify genomic risk variants in chewing-tobacco associated oral cancer patients, a genome-wide association study was conducted in patients of Indian ethnicity with long term tobacco chewing habit. We analyzed 55 oral cancer patients and 92 healthy controls for single nucleotide polymorphisms, using high throughput microarray Illumina Infinium II Assay platform and Human CNV370k-bead chip containing 370,000 single nucleotide polymorphisms. The PLINK software platform defined 298 SNPs with minor allele frequency of several genes significantly increased in oral cancer patients as compared to the controls (p < 0.001). Illumina Genome Viewer Software Version 3.2.9, further delineated 93 SNPs with p-values ranging from 9.3 x 10(-4) to 1.38 x 10(-5) and Odd's ratio of 2.18-8.48, associated with 70 genes. Analysis using Kyoto Encyclopedia of Genes and Genome Pathway database, indicated SNP association with several genes including GRIK2, RASGRP3, CAMK4, SYK, RAPTOR, FHIT, DCC, active in signal transduction; MMP2, CNTNAP2, PTPRJ associated with tumor cell migration; and apoptotic gene IRAK3. The data indicates an inherent role for the genetic constitution of individuals in oral carcinogenesis, with the genomic variants contributing to increased risk or susceptibility to oral cancer. (C) 2012 Elsevier Ltd. All rights reserved.