Axl is a member of the TAM receptor family, which also includes also MerTK and TYRO3. Axl contains protein kinase activity and is activated by dimerization and auto-phosphorylation upon ligand binding. In response to its ligands, Protein S and GAS6, Axl activates anti-inflammatory pathways (through SOCS-1 and SOCS-3), which limits TLR and cytokine signaling. This results in dampened inflammatory responses in macrophages and DCs. TAM receptors are also involved in phagocytosis of apoptotic cells. Mice lacking all three TAM receptors have several degenerative phenotypes linked to inefficient removal of apoptotic cells and membranes (e.g., in the retina and the male reproductive tract) and develop a severe autoimmune phenotype akin to systemic lupus erythematosus, including the production of broad spectrum auto-antibodies. In addition, Axl may function as a putative entry receptor for filoviruses. Axl is also used to identify a specific subpopulation of human blood dendritic cells, also referred to as Siglec 6+/Axl+ dendritic cells. Cellular expression of Axl can be upregulated by TLR ligands, such as LPS or poly I:C. Soluble Axl is generated by proteolytic cleavage of the membrane form. Increased plasma levels may be indicative of inflammation and cancer.
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Protein Aliases: Adhesion-related kinase; AXL oncogene; AXL transforming sequence/gene; AZF1; oncogene AXL; sAXL; soluble AXL; Tyrosine-protein kinase receptor UFO; ufo oncogene homolog
Gene Aliases: AI323647; ARK; AXL; JTK11; Tyro7; UFO
Molecular Function: transmembrane signal receptor