https://www.selleckchem.com/products/vx-561.html
Under mild or moderate levels of ER stress, the homeostatic UPR (hUPR) sets in motion transcriptional and translational changes that promote cell adaption and survival. However, if these processes are unsuccessful at resolving ER stress, a terminal UPR (tUPR) program dominates and actively signals cell suicide. This article summarizes the mounting evidence that cancer cells are predisposed to ER stress and vulnerable to targeted interventions against ongoing UPR signaling. PURPOSE The present study compared the postoperative pain, edema,
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