Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10907692 | Experimental Hematology | 2005 | 11 Pages |
Abstract
Our studies reveal for the first time the involvement of Src kinases in Flt3 signaling, with activation of Lyn by constitutively active Flt3 mutants as well as ligand-stimulated wild-type receptor, and show that Src kinase inhibitors block proliferative effects of Flt3 mutants found in AML. Thus, Src kinases may represent targets for inhibitor therapy in Flt3-related AML.
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Authors
Lisa J. Robinson, Jia Xue, Seth J. Corey,