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anti-Human PTPRD Antibodies:
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Mutation in PTPRD gene is associated with nodal marginal zone lymphoma.
Low PTPRD expression is associated with Head and Neck Squamous Cell Carcinoma.
The data provide evidence of the high incidence of PTPRD inactivation in laryngeal squamous cell carcinoma, suggesting that deletions and loss-of-function mutations are responsible for PTPRD loss only in a fraction of cases, whereas DNA methylation (show HELLS Antibodies) is the dominating mechanism of PTPRD inactivation.
PTPRD polymorphisms might modulate antipsychotic-induced weight gain.
PTPRD was identified as a novel locus potentially associated with blood pressure response to atenolol and resistant hypertension in multiple ethnic groups.
PTPRD mutation, but not methylation or copy number loss, may serve as a predictive biomarker of sensitivity to STAT3 (show STAT3 Antibodies) inhibitors in HNSCC.
Study shows for the first time that DNMT1 (show DNMT1 Antibodies) caused PTPRD DNA hypermethylation and induced insulin (show INS Antibodies) signaling silencing in T2D patients.
PTPRD is homozygously deleted and epigenetically downregulated in hepatocellular carcinomas (HCCs (show HCCS Antibodies)).
This study demonstrated that the copy number variations of PTPRD relate to opioid dependence.
Silencing PTPRD expression by siRNA treatment significantly enhanced cell proliferation compared with mock siRNA treatment.
Chondroitin Sulfate Proteoglycans Negatively Modulate Spinal Cord Neural Precursor Cells by Signaling Through LAR (show PTPRF Antibodies) and RPTPsigma (show PTPRS Antibodies) and Modulation of the Rho/ROCK Pathway.
Ptprd is a tumor suppressor that can promote tumorigenesis in concert with Cdkn2a (show CDKN2A Antibodies) loss.
We reveal that PTPRD is a bona fide tumor suppressor, pinpoint PTPRD loss as a cause of aberrant STAT3 (show STAT3 Antibodies) activation in gliomas, and establish PTPRD loss, in the setting of CDKN2A/p16(INK4A (show CDKN2A Antibodies)) deletion, as a driver of glioma progression.
RPTP-sigma (show PTPRS Antibodies) and RPTP-delta complement each other functionally during mammalian development, and reveal an essential contribution of RPTP-sigma (show PTPRS Antibodies) and RPTP-delta to appropriate motoneuron axon targeting during mammalian axonogenesis.
Receptor protein tyrosine phosphatase (show PTPRT Antibodies)-delta cooperates with hedgehog (show SHH Antibodies)-responsive gene MIM (show MTSS1 Antibodies) to induce cytoskeletal remodeling.
PTPRD may be one of a select group of tumor suppressor genes that are inactivated in a wide range of common tumor types.
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 contains an extracellular region, a single transmembrane segment and two tandem intracytoplasmic catalytic domains, and thus represents a receptor-type PTP. The extracellular region of this protein is composed of three Ig-like and eight fibronectin type III-like domains. Studies of the similar genes in chicken and fly suggest the role of this PTP is in promoting neurite growth, and regulating neurons axon guidance. Multiple alternatively spliced transcript variants of this gene have been reported. A related pseudogene has been identified on chromosome 5.
, protein tyrosine phosphatase, receptor type, delta polypeptide
, protein-tyrosine phosphatase delta
, receptor-type tyrosine-protein phosphatase delta