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Fig. 1 | Cell Communication and Signaling

Fig. 1

From: IDH2/R140Q mutation confers cytokine-independent proliferation of TF-1 cells by activating constitutive STAT3/5 phosphorylation

Fig. 1

TF-1(R140Q) cells were resistant to apoptosis induced by GM-CSF withdrawal. After 24 h incubation in the absence or presence of 5 ng/mL GM-CSF, TF-1(WT) and TF-1(R140Q) cells reached different densities (A) and were subjected to flow cytometry assay for apoptosis (B). C TF-1(WT) and TF-1(R140Q) cells were cultured in the absence or presence of 5 ng/mL GM-CSF for 24 h, and PARP and Bcl-xL expression levels were analyzed. GAPDH was used as a loading control (left). Normalized mean gray values of cleaved-PARP (medium) and Bcl-xL (right) in TF-1(R140Q) cells were compared with TF-1(WT) cells in the absence of 5 ng/mL GM-CSF. ***P < 0.001 compared with TF-1(WT) cells. The dose of “0” group represents the vehicle control

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