The AML1-ETO fusion gene and the
FLT3 length mutation collaborate
in inducing acute leukemia in mice
J. Clin. Invest. Christina Schessl, et al. 115:2159 doi:10.1172/JCI24225 [
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Figure 1Schematic diagram and analysis of expression of different constructs. (
A) Retroviral constructs for expression of AML1-ETO and of the AML1-ETO-L148D (
31,
47), FLT3-LM, and FLT3-LM-KD mutant proteins. The GFP vector served as a control. AE, AML1-ETO; LTR, long-terminal repeat; RHD, runt homology domain; TAF110, TATA-binding protein–associated factor 110; HHR, hydrophobic heptad repeat; ZNF, zinkfinger; TM, transmembrane; JM, juxtamembrane; PTK, protein tyrosine kinase; KI, kinase insert. (
B,
C, and
E) Western blot analysis of cellular extracts from GP
+ E86 and NIH 3T3 cells transfected with the different constructs (the molecular mass is indicated). Kasumi cells served as a positive control. (
D) α-pTyr plot demonstrating phosphorylation of FLT3-LM and FLT3-WT but not of FLT3-LM-KD. (
F) FACS analysis of Ba/F3 cells transduced with the FLT3 constructs. (
G) Growth of IL-3–dependent Ba/F3 cells infected with the different constructs. (
H and
I) Flow cytometry and RT-PCR analysis of cells coexpressing FLT3-LM/YFP and AML1-ETO/GFP, isolated from a representative leukemic mouse. FL, FLT3 ligand; PB, peripheral blood.
