Background: Chronic ER stress suppresses mTORC1 activity. Results: mTORC1-mediated suppression of translation during chronic ER stress is independent of the stress-induced eIF2α- P/ATF4 signaling. Conclusion: The eIF2α-P/ATF4-induced network of amino acid transporters promotes protein synthesis in part by increasing mTORC1-mediated translational control. Significance: The eIF2α-P/ATF4/mTORC1 network controls protein synthesis rates during chronic ER stress and mediates the degree of stress response and survival outcomes.
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cell Biology