| First Author | Ramachandran G | Year | 2021 |
| Journal | Biochem Biophys Res Commun | Volume | 534 |
| Pages | 297-302 | PubMed ID | 33272572 |
| Mgi Jnum | J:305698 | Mgi Id | MGI:6705280 |
| Doi | 10.1016/j.bbrc.2020.11.091 | Citation | Ramachandran G, et al. (2021) Optineurin modulates ER stress-induced signaling pathways and cell death. Biochem Biophys Res Commun 534:297-302 |
| abstractText | We have investigated the physiological role of the autophagy receptor Optineurin/Optn in endoplasmic reticulum (ER) stress response using cellular and animal models. In comparison to their normal counterparts, Optn-deficient mouse embryonic fibroblasts showed significantly higher cell death and caspase-3 activation upon treatment with tunicamycin and thapsigargin, inducers of ER stress. The transcript levels of some of the genes regulated by the IRE1-XBP1 and PERK-ATF4 pathways were upregulated in Optn-deficient cells, in comparison with normal cells, upon treatment with tunicamycin, and also in the brain cortex and liver of tunicamycin treated Optn-deficient mice. Also, the basal levels of IRE1alpha and PERK were higher in Optn-deficient cells. These results suggest that Optn modulates ER stress-induced signaling pathways and provides protection from ER stress-induced cell death. |
