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Anti-AXL (UFO) Antibody from rabbit, purified by affinity chromatography

ITEM#: 3042-ABN897

MFR#: ABN897

Tyrosine-protein kinase receptor UFO (EC 2.7.10.1; UniProt P30530; also known as AXL oncogene) is encoded by the AXL (also known as UFO) gene (Gene ID 558) in human. AXL/UFO, MERTK, and TYRO3 constitute the TAM family single transmembrane receptor ty

Tyrosine-protein kinase receptor UFO (EC 2.7.10.1; UniProt P30530; also known as AXL oncogene) is encoded by the AXL (also known as UFO) gene (Gene ID 558) in human. AXL/UFO, MERTK, and TYRO3 constitute the TAM family single transmembrane receptor tyrosine kinases (RTKs) similar overall domain structure, including two extracellular C2-type Ig-like domains (human AXL a.a. 27-128 & 139-222) and two type-III fibronectin domains (human AXL a.a. 227-331 & 336-428), as well as a conserved intracellular kinase domain (human AXL a.a. 536-807) with a unique KWIAIES sequence (human AXL a.a. 714-720). The activation of TAM RTKs involves lipid phosphatidylserine (PtdSer) and gamma-carboxylated proteins that interact simultaneously with TAM RTKs N-terminal region (human AXL a.a. 26-92) via their C-terminal domain and PtdSer with their N-terminus, effectively acting as "bridging ligands". Growth arrest-specific protein 6 (GAS6) and vitamin K-dependent protein S (PROS1) are the first two characterized ligands, with GAS6 targeting all three TAM RTKs and PROS1 binding only to MERTK and TYRO3. PtdSer is generally made available for TAM RTKs activation when externalized on apoptotic cell membranes, aggregating platelets, exosomes and invading virus envelopes. Additional tissue- and receptor-specific TAM RTK ligands have been identified. Unlike MERTK and TYRO3, AXL homodimerization and near-complete activation can be achieved via a 2:2 stoichiometric interaction with GAS6 without PtdSer-presenting membranes. TAM RTKs collaboratively stabilize clot formation upon their activation by PtdSer on the surface of aggregating platelets. TAM RTKs are aberrantly expressed and activated in virtually every type of cancer, where their functions in terminating innate immune-mediated inflammation and natural killer (NK) cell responses help promote cancer survival.