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Fig. 3 | Journal of Hematology & Oncology

Fig. 3

From: CRISPR/CAS9-mediated knockout of Abi1 inhibits p185Bcr-Abl-induced leukemogenesis and signal transduction to ERK and PI3K/Akt pathways

Fig. 3

Abi1 deficiency in the p185Bcr-Abl-transformed Ba/F3 cells reduced WAVE2 expression and the Bcr-Abl signaling to MAPK and PI3 kinases. a. WAVE2 expression in p185Bcr-Abl Cas9 control cells (Cas9 Ctrl) and two independent p185 Abi1 knockout cell lines (KO2.3 and KO6.2), as indicated. b. Effects of Abi1 deficiency on the p185Bcr-Abl signaling to MAPK and PI3 kinases. Upper panel: Decreased Akt serine 473 phosphorylation in Abi1 deficient p185Bcr-Abl cells. Middle panel: Abi1 deficiency inhibited p185Bcr-Abl-induced p42/44 ERK phosphorylation at threonine 202 and tyrosine 204. Bottom panel: Effects of Abi1 deficiency on p185Bcr-Abl-induced p38 MAPK phosphorylation at threonine 180 and tyrosine 182. The western blot shown is a representative of three independent experiments. c. Quantitative analysis of three independent western blots using ImageJ program. After normalized to their total protein, levels of the phosphorylated-p42/44 ERK (P-p42/44), Akt (P-Akt), and p38 MAPK (P-p38) in Cas9 Ctrl, KO6.2, and KO2.3 cells are expressed in the vertical axis as the average percentage +/- SD of that in Cas9 Ctrl cells. *P < 0.01 and **P = 0.31 as compared to Cas9 control cells

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