Tyrosine-protein kinase receptor UFO is an enzyme that in humans is encoded by the AXL gene. The gene was initially designated as UFO, in allusion to the unidentified function of this protein. The AXL protein is a cell surface receptor.
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Gene and protein structure
The Axl gene is evolutionarily conserved between vertebrate species. This gene has two different alternatively spliced transcript variants.
The protein encoded by this gene is a member of the receptor tyrosine kinase subfamily. Although it is similar to other receptor tyrosine kinases, the Axl protein represents a unique structure of the extracellular region that juxtaposes IgL and FNIII repeats.
Function
The AXL receptor transduces signals from the extracellular matrix into the cytoplasm by binding growth factors like vitamin K-dependent protein growth-arrest-specific gene 6 (GAS6). It is involved in the stimulation of cell proliferation.
This receptor can also mediate cell aggregation by homophilic binding.
Axl is an essential epithelial-to-mesenchymal transition-induced regulator of breast cancer metastasis and patient survival.
Clinical significance
Axl is a chronic myelogenous leukemia-associated oncogene and also associated with colon cancer and melanoma. It is in close vicinity to the BCL3 oncogene, which is at 19q13.1-q13.2.
AXL may play an important role in Zika virus infection, allowing for entry of the virus into host cells.
As a drug target
Cancer
There is ongoing research to develop possible drugs to target this signalling pathway and treat cancers. In 2014 those in clinical trials included: LY2801653, MP-470 (Amuvatinib), SKI-606 (Bosutinib), MGCD 265, ASP2215, XL184 (Cabozantinib), GSK1363089/XL880 (Foretinib), SGI-7079, and R428 (BGB324).
e.g. Astellas Pharma is currently testing ASP2215 (Gilteritinib), a dual FLT3-AXL tyrosine kinase inhibitor in acute myeloid leukemia (AML).
BGB324 (a selective AXL inhibitor) is in clinical trials for AML and non-small cell lung cancer (NSCLC).
Interactions
AXL receptor tyrosine kinase has been shown to interact with TENC1.
Source of the article : Wikipedia
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