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: Phosphatase; Motility/polarity/chemotaxis; Protein phosphatase, tyrosine (non-receptor); EC 188.8.131.52
Molecular Function: enzyme binding; ephrin receptor binding; insulin receptor binding; protein binding; protein kinase binding; protein phosphatase 2A binding; protein tyrosine phosphatase activity; receptor tyrosine kinase binding; zinc ion binding
Biological Process: actin cytoskeleton reorganization; activation of JNK activity; blood coagulation; cytokine and chemokine mediated signaling pathway; insulin receptor signaling pathway; negative regulation of insulin receptor signaling pathway; negative regulation of MAP kinase activity; negative regulation of vascular endothelial growth factor receptor signaling pathway; platelet activation; protein amino acid dephosphorylation; regulation of endocytosis; regulation of intracellular protein transport; regulation of signal transduction; unfolded protein response; unfolded protein response, activation of signaling protein activity
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.