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. 2018 Sep 5;131(17):jcs217760. doi: 10.1242/jcs.217760

Fig. 7.

Fig. 7.

The PERK branch of the UPR is activated in response to MAL3-101. (A) RMS13-R and RMS13 cells were treated with MAL3-101 for 4 h in the presence or absence of the IRE1 inhibitor 4µ8C and the accumulation of the unspliced and spliced XbpI (XbpIu and XbpIs) mRNAs were monitored by PCR. (B) RMS13-R and RMS13 cells were treated with MAL3-101 to detect the full-length and cleaved forms of ATF6. A 1 h DTT treatment was used as a positive control. (C) RMS13-R and RMS13 cells were treated with the indicated compounds or with DMSO for 4 h and PERK phosphorylation (p-PERK) was monitored by immunoblotting. p-PERK accumulation is detected upon MAL3-101 or MAL3-101/CQ treatment. A 1 h DTT treatment was used as a positive control. (D) ATF4 is degraded more rapidly in RMS13-R cells. The RMS13-R and RMS13 cells were pre-treated with MAL3-101 for 3 h and then cycloheximide was added for the indicated times. Lysates were resolved by SDS-PAGE and immunoblotted for ATF4. Graphs represent the mean± s.d. of three independent experiments. **P<0.005, ***P<0.0001.