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. 2022 Aug 17;25(4):735–747. doi: 10.1093/neuonc/noac199

Fig. 4.

Fig. 4

On-target activity and cell death induction upon BCL-XLi treatment. (OIS (-DOX): oncogene-induced senescence; 5 days doxycycline withdrawal). (A) Western blot of BCL-XL and BAK after immunoprecipitation (IP) of BCL-XL after 4 h treatment of PA cells in OIS with 1 µM navitoclax. (B) Relative viable attached cells after 72 h of drug treatment (mean ± SD, n = 3 biological replicates). Grey boxes indicate drugs' inhibitory profiles (Ki < 1 nM). Unpaired t-test: *P < .05, **P < .01, ***P < .001. ****P < .0001 (comparison to DMSO). (C) Loss of mitochondrial membrane potential (MMP) measured by TMRE incorporation after 24 h treatment (mean ± SD, n = 3). Unpaired t-test. *P < .05, **P < .01, ***P < .001 (comparison to DMSO). (D) Relative caspase 3 activity after 24 h of treatment with 100 nM navitoclax or 100 nM A-1331852, control: DMSO (mean ± SD, n=3). (E) Relative viable cells 14 days after BCL-XL knock-down (100%: control shRNA) (mean ± SD, n=3). *Tukey multiple comparisons of means adjusted P-value < .01. (F, G) Relative cytochrome c released into the cytosol after 1 h of treatment with 10 µM BAD peptide (F) or 100 µM HRK peptide (G), respectively, relative to DMSO (mean ± SD, n = at least 3). rel.: relative; c: concentration.