GIV/Girdin promotes cell survival during endoplasmic reticulum stress
Abstract
Endoplasmic reticulum (ER) stress is a form of cellular stress that is experienced by cells both under normal physiological conditions such as in professional secretory cells and disease states such as cancer, diabetes, and neurodegeneration. Upon facing ER stress, cells activate a conserved signaling pathway called the unfolded protein response (UPR) to restore normal function by halting general protein translation, upregulating expression of chaperones, and promoting ER-associated degradation. However, if the stress is overwhelming and cells are not able to recover within a reasonable time frame, the UPR ultimately commits cells to programmed cell death. How cells make this life-or-death decision remains an exciting yet poorly understood phenomenon. Here, we show that Gα-interacting vesicle-associated protein (GIV) aka Girdin plays an important role in promoting cell survival during ER stress. Cells lacking GIV are impaired in activating the pro-survival Akt pathway upon induction of ER stress. These cells also show enhanced levels of the pro-apoptotic transcription factor, CCAAT/enhancer binding protein homologous protein (CHOP) as compared to control cells. Due to decreased pro-survival signals and a concomitant increase in...Continue Reading
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