loss of PTPRS expression may predict an aggressive clinical course in ESCC patients. PTPRS may function as a tumor suppressor and play an important role in esophageal squamous cell carcinoma growth and metastasis
Study identified several CpG sites and specifically several CpGs in the PTPRS and PER3 genes differentially methylated between obese and non-obese children suggesting a role for DNA methylation concerning development of childhood obesity.
represents an evolutionarily conserved pDC-specific inhibitory receptor and is required to prevent spontaneous IFN production and immune-mediated intestinal inflammation
Data demonstrate that synoviocytes are regulated by an RPTPsigma-dependent proteoglycan switch in vivo which can be targeted for rheumatoid arthritis therapy.
Receptor protein tyrosine phosphatase sigma (RPTPsigma) regulates neuronal extension and acts as a presynaptic nexus for multiple protein and proteoglycan interactions during synaptogenesis.
Intragenic microdeletions of the EGFR phosphatase PTPRS were found frequently (26%) in head and neck cancers identifying this gene as a target of 19p13 loss.
crystallographic analyses of a shared HSPG-CSPG binding site reveal a conformational plasticity that can accommodate diverse glycosaminoglycans with comparable affinities; HS and analogs induced RPTPsigma ectodomain oligomerization which was inhibited by CS
Trans-synaptic adhesions between netrin-G ligand-3 (NGL-3) and receptor tyrosine phosphatases LAR protein-tyrosine phosphatase delta (PTPdelta) and PTPsigma via specific domains regulate excitatory synapse formation.
Observational study of gene-disease association. (HuGE Navigator); In colorectal tumors microsatellite repeats mutation rates are higher than the mean mutation frequency
SNPs rs1143699 rs4807015 and rs1978237 confer an increased risk of developing type 2 diabetes mellitus; Observational study of gene-disease association. (HuGE Navigator)
Three SNPs that flank exon 8 are associated with ulcerative colitis. The presence of these SNPs is associated with novel splicing that removes the third immunoglobulin-like domain (exon 9) from the extracellular portion of PTPsigma.
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