AXL is a member of the receptor tyrosine kinase family which has oncogenic potential and is implicated in human myeloid leukemia. AXL is a member of a complex signaling network that is involved in the control of cell proliferation and differentiation. Overexpression of AXL cDNA in NIH 3T3 cells induces neoplastic transformation of these cells with the concomitant appearance of a 140 kDa AXL tyrosine-phosphorylated protein. Expression of AXL cDNA in the baculovirus system results in the expression of the appropriate recombinant protein that is recognized by antiphosphotyrosine antibodies, confirming that the AXL protein is tyrosine phosphorylated.
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We have detected transforming activity by a tumorigenicity assay using NIH3T3 cells transfected with DNA from a chronic myeloproliferative disorder patient. Here, we report the cDNA cloning of the corresponding oncogene, designated UFO, in allusion to the as yet unidentified
Molecular and cellular biology, 11(10), 5016-5031 (1991-10-01)
Using a sensitive transfection-tumorigenicity assay, we have isolated a novel transforming gene from the DNA of two patients with chronic myelogenous leukemia. Sequence analysis indicates that the product of this gene, axl, is a receptor tyrosine kinase. Overexpression of axl
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