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Validated All-in-One™ qPCR Primer for PTPRJ(NM_002843.3) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
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. [provided by RefSeq].
Gene References into function
- In this paper, frequent deletion of PTPRJ is shown in human colon, lung, and breast cancers.
- This protein is frequently deleted in human breast cancers.
- CD148 and CD27 are expressed in a wide range of B cell non-Hodgkin's lymphomas and do not serve to distinguish between neoplastic cells of naive and memory B cell derivation
- DEP-1 is a negative regulator of cell proliferation, cell-substratum contacts, motility and chemotaxis in fibroblasts
- propose that the expression and activation of DEP-1/PTPeta is required for somatostatin inhibition of glioma proliferation
- A candidate tumor suppressor gene because its expression was blocked in rat and human thyroid transformed cells, and its restoration reverted their neoplastic phenotype.
- genotypic profile of PTPRJ affects susceptibility to thyroid carcinomas, loss involved in thyroid carcinogenesis
- single nucleotide polymorphisms in protein tyrosine phosphatase receptor type J is associated with breast cancer
- Male, dizygotic twins were diagnosed with sensori-neural deafness at ages 5 and 21 months and later developed hypothyroidism at ages 24 and 28 months, respectively. Analysis for anti-DEP-1/CD148 autoantibodies described in Cogan syndrome proved positive.
- Chemoprotective nutrients elevated transcription of endogenous DEP-1 mRNA & expression of DEP-1 protein. Upregulation of DEP-1 expression & inhibition of cell growth & migration may be a previously unrecognized mechanism of chemoprevention by nutrients.
- Findings identify RET as a novel substrate of PTPRJ and suggest that PTPRJ expression levels may affect tumor phenotype associated with RET/PTC1 and RET(C634R) mutants.
- These results demonstrate that CD148 may interact with and dephosphorylate p85 when it is phosphorylated and modulate the magnitude of phosphoinositide 3-kinase activity.
- The translation of the region between AUG(191) and AUG(356) inhibits the overall expression of PTPRJ mRNA.
- No significant evidence for the A1176C allele of PTPRJ or previously described haplotypes of tagSNPs in PTPRJ on CRC risk.
- DEP-1 is a positive regulator of VEGF-mediated Src and Akt activation and endothelial cell survival.
