MTOR inhibition increases cell viability via autophagy induction during endoplasmic reticulum stress - An experimental and modeling study.

ABSTRACT: Unfolded or misfolded proteins in the endoplasmic reticulum (ER) trigger an adaptive ER stress response known as unfolded protein response (UPR). Depending on the severity of ER stress, either autophagy-controlled survival or apoptotic cell death can be induced. The molecular mechanisms by which UPR controls multiple fate decisions have started to emerge. One such molecular mechanism involves a master regulator of cell growth, mammalian target of rapamycin (mTOR), which paradoxically is shown to have pro-apoptotic role by mutually interacting with ER stress response. How the interconnections between UPR and mTOR influence the dynamics of autophagy and apoptosis activation is still unclear. Here we make an attempt to explore this problem by using experiments and mathematical modeling. The e

SUBMITTER: Kapuy O 

PROVIDER: S-EPMC4141208 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature