Figure 2.
AXL is constitutively activated in MCL cell lines and patient cells. (A) Western blot studies demonstrated the phosphorylation of AXL in all MCL cell lines. (B) JeKo-1 cells were treated with bemcentinib at concentrations ranging from 0.5 to 4 μM. Phosphorylation of AXL was evaluated using a p-AXL antibody. Bemcentinib treatment reduces the level of AXL phosphorylation in MCL cells. (C) AXL phosphorylation status was evaluated in cells from patients with MCL by western blot. The AXL phosphorylation was detectable in all patient–derived MCL cells. The results also indicated that AXL3 is the isoform predominantly activated in primary MCL cells. In contrast, CD19+ B cells from healthy individuals present a weak AXL activation and the complete absence of AXL3 phosphorylation. Experiments were performed in triplicate.

AXL is constitutively activated in MCL cell lines and patient cells. (A) Western blot studies demonstrated the phosphorylation of AXL in all MCL cell lines. (B) JeKo-1 cells were treated with bemcentinib at concentrations ranging from 0.5 to 4 μM. Phosphorylation of AXL was evaluated using a p-AXL antibody. Bemcentinib treatment reduces the level of AXL phosphorylation in MCL cells. (C) AXL phosphorylation status was evaluated in cells from patients with MCL by western blot. The AXL phosphorylation was detectable in all patient–derived MCL cells. The results also indicated that AXL3 is the isoform predominantly activated in primary MCL cells. In contrast, CD19+ B cells from healthy individuals present a weak AXL activation and the complete absence of AXL3 phosphorylation. Experiments were performed in triplicate.

Close Modal

or Create an Account

Close Modal
Close Modal