Mer
a proto-oncogene receptor tyrosine-protein kinase of the Axl family. Binds several ligands including LGALS3, Tubby, TULP1 or GAS6. Regulates many physiological processes including cell survival, migration, differentiation, and phagocytosis of apoptotic cells (efferocytosis). Functions in the retinal pigment epithelium (RPE) as a regulator of rod outer segments fragments phagocytosis. 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.
Interacts (upon activation) with TNK2; stimulates TNK2 autophosphorylation. Interacts with VAV1 in a phosphotyrosine-independent manner. Not expressed in normal B- and T-lymphocytes but is expressed in numerous neoplastic B- and T-cell lines. Highly expressed in testis, ovary, prostate, lung, and kidney, with lower expression in spleen, small intestine, colon, and liver. Defects are a cause of retinitis pigmentosa, a group of human diseases that leads to degeneration of retinal photoreceptor cells. Note: This description may include information from UniProtKB.
Protein type: Kinase, protein; Protein kinase, tyrosine (receptor); Protein kinase, TK; EC 2.7.10.1; Membrane protein, integral; TK group; Axl family
Cellular Component: extracellular space; photoreceptor outer segment; integral to plasma membrane; cytoplasm; plasma membrane
Molecular Function: protein binding; transmembrane receptor protein tyrosine kinase activity; ATP binding
Biological Process: negative regulation of lymphocyte activation; platelet activation; vagina development; protein amino acid phosphorylation; phagocytosis; cell surface receptor linked signal transduction; cell-cell signaling; natural killer cell differentiation; retina development in camera-type eye; positive regulation of phagocytosis; protein kinase B signaling cascade; spermatogenesis; blood coagulation; leukocyte migration; 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.
