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. Author manuscript; available in PMC: 2012 Oct 1.
Published in final edited form as: Exp Hematol. 2011 Jul 1;39(10):999–1006. doi: 10.1016/j.exphem.2011.06.007

Figure 4.

Figure 4

Schematic representation of the molecular mechanisms by which resveratrol induces the pro-apoptotic effects of ER stress responses and represses the cell survival signals (XBP1s signaling) in MM. Resveratrol increases ER stress and the 3 main pathway branches PERK, ATF6, and IRE1α. This results in activation of cell death signals via IRE1α activation of JNK and PERK and ATF6 activation of CHOP. While activation of IRE1α also results in increased XBP1s, resveratrol specifically inhibits the transcriptional activity of XBP1s, which leads to impairment of the cell survival functions and promotes cell death.