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.
Paula LindnerSøren Brøgger ChristensenPoul NissenJesper Vuust MøllerNikolai EngedalPublished in: Cell communication and signaling : CCS (2020)
Together, our results provide a new, integrated understanding of UPR signaling mechanisms and downstream mediators that induce cell death upon Tg-triggered, unmitigated ER stress. Video Abstract.