Table 2. wrwycr does not induce the ER stress response in HeLa cells.
| Treatments | pGRP78a | pSV40b | pGRP78/pSV40d | ||
| Units | Fold change | Units | Fold change | ||
| DMSO | 118163±1459 | 60627±3016 | |||
| 100 µM wrwycr | 184755±11572 | 1.53±0.09 | 112162±4444 | 1.9±0.17 | 0.84±0.1 |
| 150 µM wrwycr | 214642±18292 | 1.8±0.1 | 135441±32099 | 2.9±0.05 | 1.02±0.44 |
| 200 µM wrwycr | 282941±27749 | 2.4±0.2 | 165928±1165 | 2.7±0.09 | 0.87±0.06 |
| wkhyny | 62097±1715 | 0.50±0.02 | 56685±1657 | 0.9±0.02 | 0.55±0.01 |
| Tunicamycinc | 425255±16205 | 7.9±0.09 | 4606±362.1 | 0.4±0.02 | 20.0±1.36 |
a
plasmid DJT208 carries the GRP78 promoter (pGRP78) which drives the ER-stress response elements ERSE 1, ERSE 2 and ERSE 3 upstream of the luciferase gene.
b
plasmid pGL2P carries the luciferase gene driven by the SV40 promoter (pSV40).
c
Tunicamycin, a known inducer of ER stress, was used as a positive control.
d
ER stress was calculated as the fold increase of luciferase gene expression from the GRP78 promoter over that from the SV40 promoter of pGL2P for the different concentrations of the peptide over DMSO or over the media in the case of TM.