Anti-MerTK (Innate Immune Checkpoint) Monoclona Antibody (Clone: MERTK/3015)

MerTK, also called c-Mer, is a member of the Mer/Axl/Tyro3 receptor kinase family. It is a 984 residue transmembrane protein made up of one tyrosine kinase domain, two Fibronectin type-III domains and two immunoglobulinlike C2-type domains. MerTK is the mammalian ortholog of the chicken retroviral oncogene product v-Eyk. This protein plays a critical role in macrophage activation, platelet aggregation, clot stability and the efficient removal of apoptotic cells. Specifically, MerTK acts as a signaling molecule, triggering outer segment ingestion in the retinal pigment epithelium (RPE) phagocytic process. Evidence suggests that MerTK signals via interaction with phosphatidylinositol-specific phospholipase C 2). When the gene encoding for MerTK is mutated, the RPE phagocytosis pathway is disrupted and autosomal recessive retinitis pigmentosa (RP) may result, leading to degeneration of retinal photoreceptor cells. Protein function: Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding to several ligands including LGALS3, TUB, TULP1 or GAS6. Regulates many physiological processes including cell survival, migration, differentiation, and phagocytosis of apoptotic cells (efferocytosis). Ligand binding at the cell surface induces autophosphorylation of MERTK on its intracellular domain that provides docking sites for downstream signaling molecules. Following activation by ligand, interacts with GRB2 or PLCG2 and induces phosphorylation of MAPK1, MAPK2, FAK/PTK2 or RAC1. MERTK signaling plays a role in various processes such as macrophage clearance of apoptotic cells, platelet aggregation, cytoskeleton reorganization and engulfment. 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. [The UniProt Consortium]