Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding to several ligands including TUB, TULP1 or GAS6. Regulates many physiological processes including cell survival, migration and differentiation. Ligand binding at the cell surface induces dimerization and autophosphorylation of TYRO3 on its intracellular domain that provides docking sites for downstream signaling molecules. Following activation by ligand, interacts with PIK3R1 and thereby enhances PI3-kinase activity. Activates the AKT survival pathway, including nuclear translocation of NF-kappa-B and up-regulation of transcription of NF-kappa-B-regulated genes. TYRO3 signaling plays a role in various processes such as neuron protection from excitotoxic injury, platelet aggregation and cytoskeleton reorganization. Plays also an important role in inhibition of Toll-like receptors (TLRs)-mediated innate immune response by activating STAT1, which selectively induces production of suppressors of cytokine signaling SOCS1 and SOCS3. Monomer and homodimer. Interacts (via N-terminus) with extracellular ligands TUB, TULP1 and GAS6. Interacts with PIK3R1; this interaction increases PI3-kinase activity. Abundant in the brain and lower levels in other tissues. Belongs to the protein kinase superfamily. Tyr protein kinase family. AXL/UFO subfamily. Note: This description may include information from UniProtKB.
Protein type: Kinase, protein; EC 220.127.116.11; Protein kinase, TK; EC 18.104.22.168; Protein kinase, tyrosine (receptor); Membrane protein, integral; TK group; Axl family
Cellular Component: endoplasmic reticulum membrane; integral to plasma membrane; nuclear envelope; nucleus
Molecular Function: protein binding; protein heterodimerization activity; protein-tyrosine kinase activity; phosphoinositide 3-kinase binding; receptor signaling protein tyrosine kinase activity; transmembrane receptor protein tyrosine kinase activity; ATP binding
Biological Process: forebrain cell migration; negative regulation of lymphocyte activation; platelet activation; phosphoinositide 3-kinase cascade; protein amino acid autophosphorylation; vagina development; signal transduction; ovulation cycle; natural killer cell differentiation; negative regulation of innate immune response; negative regulation of inflammatory response; protein kinase B signaling cascade; negative regulation of toll-like receptor signaling pathway; spermatogenesis; negative regulation of neuron apoptosis; cell adhesion; apoptotic cell clearance; secretion by cell
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.