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Recombinant Mouse MERTK/MER Protein (His & GST Tag) (PKSM040301)

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50μg $ 580.00
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For research use only.

Synonyms Eyk, Mer, Nyk, nmf12
Species Mouse
Expression Host Baculovirus-Insect Cells
Sequence Glu573-Tyr867
Accession Q60805
Calculated Molecular Weight 61.7 kDa
Observed Molecular Weight 58 kDa
Tag N-His-GST
Bio-activity The specific activity was determined to be 30 nmol/min/mg using Poly(Glu, Tyr) 4:1 as substrate.
Purity > 96 % as determined by reducing SDS-PAGE.
Endotoxin < 1.0 EU per μg of the protein as determined by the LAL method.
Storage Store at < -20°C, stable for 6 months. Please minimize freeze-thaw cycles.
Shipping This product is provided as liquid. It is shipped at frozen temperature with blue ice/gel packs. Upon receipt, store it immediately at < - 20°C.
Formulation Supplied as sterile solution of 20mM Tris, 500mM NaCl, pH 7.4, 10% glycerol
Reconstitution Not Applicable
Background 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 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 testis, ovary, prostate, lung, and kidney, with lower expression in 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 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. Defects in MERTK are the cause of retinitis pigmentosa type 38.
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