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Fig. 4 | Cell Communication and Signaling

Fig. 4

From: Targeting of the AXL receptor tyrosine kinase by small molecule inhibitor leads to AXL cell surface accumulation by impairing the ubiquitin-dependent receptor degradation

Fig. 4

BMS777607 (BMS) is influencing the lysosomal degradation pathway. Hs578T cells were treated with 0.5 μM BMS or 2 μM BB94 in combination with 1 μM DAPT or 1/10 μM CQ for 24 h. DAPT stabilized the 55 kDa C-terminal AXL fragment by inhibition of further degradation by γ-secretases. The α-secretase inhibitor BB94 decreased the abundance of the 55 kDa C-terminal AXL fragment by blocking the AXL receptor shedding. BMS in contrast to BB94 increased the abundance of the 55 kDa C-terminal AXL fragment, indicating that the increased abundance of the 140 kDa AXL is not caused by off-target α-secretase inhibition. 10 μM CQ stabilized a 54 kDa C-terminal AXL fragment by inhibition of lysosomal acidification. BMS reduced the abundance of the 54 kDa C-terminal AXL fragment suggesting that BMS influenced the lysosomal degradation pathway

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