Additional file 6 of Cell death induced by the ER stressor thapsigargin involves death receptor 5, a non-autophagic function of MAP1LC3B, and distinct contributions from unfolded protein response components

Autor: Lindner, Paula, Christensen, Søren, Nissen, Poul, Møller, Jesper, Engedal, Nikolai
Rok vydání: 2020
Předmět:
DOI: 10.6084/m9.figshare.11742105
Popis: Additional file 5: Figure S12. Tg-mediated upregulation of DR5- and LC3B mRNA levels requires PERK, ATF4 and CHOP in LNCaP and HCT116 cells. Figure S13. IRE1 and ATF6 knockdown confirmations (related to Fig. 5). Figure S14. Tg-mediated caspase activation and upregulation of DR5 and LC3B does not require IRE1, XBP1, ATF6, or JNK in HCT116 cells. Figure S15. Tg rapidly enhances XBP1s mRNA levels in an IRE1-dependent manner in LNCaP cells (related to Fig. 8). Figure S16. Cell death induced by the therapeutically relevant Tg analogs Leu-8ADT and βAsp-8ADT requires DR5 and caspase-8 in LNCaP and HCT116 cells, and partially requires FADD and Fas in LNCaP cells, whereas DR4 and TRADD are not required in any of the cell lines. Figure S17. Cell death induced by Leu-8ADT and βAsp-8ADT requires PERK, ATF4, and CHOP in LNCaP and HCT116 cells. Figure S18. Cell death induced by Leu-8ADT and βAsp-8ADT involves IRE1, XBP1, and JNK in LNCaP, but not HCT116 cells.
Databáze: OpenAIRE