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. 2014 Sep 9;33(20):2374–2387. doi: 10.15252/embj.201488648

Figure 1. Trisomic and tetrasomic human cell lines show defects in protein folding.

Figure 1

A–D Refolding of the sensor proteins upon heat shock in control cells and in respective aneuploids. HCT116 and HCT116* stably expressing histone H2B-GFP and their aneuploid derivatives were transfected either with FlucWT-mCherry (A, B) or FlucDM-mCherry (C, D) and subjected to heat stress for 2 h at 43°C. Controls were maintained at 37°C. Luminescence readings were taken immediately from heat-stressed cells (0 min) and at indicated time points after recovery at 37°C. The luminescence values of control cells maintained at 37°C were set to 100% (indicated by dotted line).

E, F Refolding of the sensor proteins upon HSP90 inhibition in control cells and in respective aneuploids. FlucWT-mCherry or FlucDM-mCherry was expressed in parental and aneuploid HCT116 or HCT116* (E) and RPE-1 or RPE-1* (F) cell lines for 36 h. Cells were then incubated with either solvent control (DMSO) or 50 nM 17-AAG for 8 h followed by measurement of luminescent activity. The depicted values show the percentage of luminescence in cells treated with 17-AAG relative to DMSO-treated cells (which were set to 100%).

Data information: All plots show the means of at least three independent experiments ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; non-parametric t-test.