a SH2-containing a ubiquitously expressed tyrosine-specific protein phosphatase. It participates in signaling events downstream of receptors for growth factors, cytokines, hormones, antigens and extracellular matrices in the control of cell growth, differentiation, migration, and death. Activation of SHP-2 and its association with Gab1 is critical for sustained Erk activation downstream of several growth factor receptors and cytokines. Note: This description may include information from UniProtKB.
Protein type: Protein phosphatase, tyrosine (non-receptor); EC 22.214.171.124; Motility/polarity/chemotaxis
Cellular Component: protein complex; mitochondrion; cytoplasm; cytosol
Molecular Function: protein domain specific binding; protein binding; phospholipase binding; SH3/SH2 adaptor activity; peptide hormone receptor binding; insulin receptor substrate binding; non-membrane spanning protein tyrosine phosphatase activity; protein tyrosine phosphatase activity; receptor tyrosine kinase binding; insulin receptor binding
Biological Process: axon guidance; hormone-mediated signaling; nerve growth factor receptor signaling pathway; activation of MAPK activity; reproductive process in a multicellular organism; glucose homeostasis; regulation of protein export from nucleus; negative regulation of insulin secretion; regulation of cell adhesion mediated by integrin; ephrin receptor signaling pathway; negative regulation of growth hormone secretion; epidermal growth factor receptor signaling pathway; fibroblast growth factor receptor signaling pathway; cytokine and chemokine mediated signaling pathway; positive regulation of hormone secretion; regulation of multicellular organism growth; negative regulation of cortisol secretion; organ growth; triacylglycerol metabolic process; DNA damage checkpoint; T cell costimulation; insulin receptor signaling pathway; hormone metabolic process; blood coagulation; leukocyte migration
SS: 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.