Endoplasmic reticulum (ER) stress and activation of the unfolded protein response inhibits de novo protein translation and activates CHOP. However, the long-term induction of these pathways in response to prolonged ER stress would be detrimental. Tabas and colleagues now reveal a mechanism through which Toll-like receptor signalling suppresses CHOP activation and promotes protein translation, thus allowing cells to adapt to persistent ER stress.
- Connie W. Woo
- Lydia Kutzler
- Ira Tabas
