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MER / MERTK

c-mer proto-oncogene tyrosine kinase

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.

Gene Name: c-mer proto-oncogene tyrosine kinase
Family/Subfamily: Protein Kinase , Axl
Synonyms: MERTK, Eyk, MER, MER receptor tyrosine kinase, Nyk, Proto-oncogene c-Mer, RP38, STK kinase, C-mer, Receptor tyrosine kinase MerTK, Tyrosine-protein kinase Mer
Target Sequences: NM_006343 NP_006334.2 Q12866

Publications (1)

1
MicroRNA-126 overexpression rescues diabetes-induced impairment in efferocytosis of apoptotic cardiomyocytes. Suresh Babu S, Thandavarayan RA, Joladarashi D, Jeyabal P, Krishnamurthy S, Bhimaraj A, Youker KA, Krishnamurthy P. Scientific reports. 2016 6:36207. (WB; Human) [Full Text Article] [PubMed:27827458] [PMC:PMC5101812]

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The data on this page has been compiled from LifeSpan internal sources, the National Center for Biotechnology Information (NCBI), and The Universal Protein Resource (UniProt).