a non-receptor phospho-tyrosine protein phosphatase which acts as a regulator of endoplasmic reticulum unfolded protein response. Mediates dephosphorylation and inactivation of PERK. May play an important role in CKII- and p60c-src-induced signal transduction cascades. May regulate the EFNA5-EPHA3 signaling pathway which modulates cell reorganization and cell-cell repulsion. Negatively regulates insulin signaling by dephosphorylating the phosphotyrosine residues of insulin receptor. Also reported to dephosphorylate integrin, epidermal growth factor receptor, JAK2 and TYK2, regulating cell growth control and the cellular response to interferon. May regulate the hepatocyte growth factor receptor signaling pathway through dephosphorylation of MET. PTP1B knockout mice show resistance to dietary weight gain and enhanced insulin sensitivity, suggesting a possible role in treatment of obesity as well as type 2 diabetes. Note: This description may include information from UniProtKB.
Protein type: EC 126.96.36.199; Motility/polarity/chemotaxis; Protein phosphatase, tyrosine (non-receptor); Phosphatase
Molecular Function: protein binding; enzyme binding; ephrin receptor binding; zinc ion binding; protein phosphatase 2A binding; protein tyrosine phosphatase activity; receptor tyrosine kinase binding; protein kinase binding; insulin receptor binding
Biological Process: negative regulation of MAP kinase activity; platelet activation; negative regulation of vascular endothelial growth factor receptor signaling pathway; unfolded protein response; cytokine and chemokine mediated signaling pathway; negative regulation of insulin receptor signaling pathway; regulation of signal transduction; protein amino acid dephosphorylation; activation of JNK activity; unfolded protein response, activation of signaling protein activity; regulation of intracellular protein transport; actin cytoskeleton reorganization; regulation of endocytosis; insulin receptor signaling pathway; blood coagulation
LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.