Kinase activity untested

Mer Protein, Human, Recombinant (aa 578-872) is expressed in Baculovirus insect cells. The predicted molecular weight is 34.1 kDa and the accession number is Q12866.

Human

Baculovirus Insect Cells

Tyro12,RP38,MER proto-oncogene, tyrosine kinase,MER,c-mer,c-Eyk

A DNA sequence encoding the human MERTK (Q12866) (Glu 578-Tyr 872) was expressed and purified with two additional amino acids (Gly & Pro ) at the N-terminus. Predicted N terminal: Gly

> 85 % as determined by SDS-PAGE

A Certificate of Analysis (CoA) containing reconstitution instructions is included with the products. Please refer to the CoA for detailed information.

It is recommended to store the product under sterile conditions at -20°C to -80°C. Samples are stable for up to 12 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.

Proto-oncogene tyrosine-protein kinase MER (MERTK) is a member of the MER/AXL/TYRO3 receptor kinase family and encodes a transmembrane protein with two fibronectin type-III domains, two Ig-like C2-type (immunoglobulin-like) domains, and one tyrosine kinase domain. MERTK is localized in the membrane and is no expressed in normal B- and T-lymphocytes but is expressed in numerous neoplastic B- and T-cell lines. This protein is highly expressed in the testis, ovary, prostate, lung, and kidney, with lower expression in the spleen, small intestine, colon, and liver. MERTK 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. MERTK signaling plays a role in various processes such as macrophage clearance of apoptotic cells, platelet aggregation, cytoskeleton reorganization, and engulfment. MERTK plays also an important role in the inhibition of Toll-like receptors (TLRs)-mediated innate immune response by activating STAT1, which selectively induces the production of suppressors of cytokine signaling SOCS1 and SOCS3. Defects in MERTK are the cause of retinitis pigmentosa type 38.