PMID: 19651891 Free PMC article.Īn efficient ribosomal frame-shifting signal in the polymerase-encoding region of the coronavirus IBV. Julie Hollien, Jonathan H Lin, +3 authors, Han Li, Nicole Stevens, Peter Walter, Jonathan S Weissman. Regulated Ire1-dependent decay of messenger RNAs in mammalian cells. The biological relationship of mouse hepatitis virus (MHV) strains and interferon: in vitro induction and sensitivities.Īrch Virol, 1984 Jan 01 82(1-2). Tarik Asselah, Ivan Bièche, +14 authors, Abdellah Mansouri, Ingrid Laurendeau, Dominique Cazals-Hatem, Gérard Feldmann, Pierre Bedossa, Valérie Paradis, Michelle Martinot-Peignoux, Didier Lebrec, Cécile Guichard, Eric Ogier-Denis, Michel Vidaud, Zéra Tellier, Vassili Soumelis, Patrick Marcellin, Richard Moreau. In vivo hepatic endoplasmic reticulum stress in patients with chronic hepatitis C.
Hamsa Puthalakath, Lorraine A O'Reilly, +11 authors, Priscilla Gunn, Lily Lee, Priscilla N Kelly, Nicholas D Huntington, Peter D Hughes, Ewa M Michalak, Jennifer McKimm-Breschkin, Noburo Motoyama, Tomomi Gotoh, Shizuo Akira, Philippe Bouillet, Andreas Strasser. PMID: 21841196 Free PMC article.ĮR stress triggers apoptosis by activating BH3-only protein Bim.
Nobuhiro Morishima, Keiko Nakanishi, Akihiko Nakano. PMID: 21959016 Free PMC article.Īctivating transcription factor-6 (ATF6) mediates apoptosis with reduction of myeloid cell leukemia sequence 1 (Mcl-1) protein via induction of WW domain binding protein 1. Ying Liao, Xiaoxing Wang, +2 authors, Mei Huang, James P Tam, Ding Xiang Liu. Regulation of the p38 mitogen-activated protein kinase and dual-specificity phosphatase 1 feedback loop modulates the induction of interleukin 6 and 8 in cells infected with coronavirus infectious bronchitis virus. H Yoshida, T Okada, +4 authors, K Haze, H Yanagi, T Yura, M Negishi, K Mori. In this review, we summarize the current knowledge on coronavirus-induced ER stress and UPR activation, with emphasis on their cross-talking to apoptotic signaling.ĮR stress apoptosis coronavirus proinflammatory cytokines signal transduction pathways unfolded protein response.Įndoplasmic reticulum stress-induced formation of transcription factor complex ERSF including NF-Y (CBF) and activating transcription factors 6alpha and 6beta that activates the mammalian unfolded protein response. ER stress and UPR activation may therefore contribute significantly to the viral replication and pathogenesis during coronavirus infection. Activation of the three branches of UPR modulates a wide variety of signaling pathways, such as mitogen-activated protein (MAP) kinase activation, autophagy, apoptosis, and innate immune response. Accumulating evidence from recent studies has shown that induction of ER stress and UPR may constitute a major aspect of coronavirus-host interaction. However, under prolonged ER stress, UPR can also induce apoptotic cell death. Coronavirus infection of cultured cells was previously shown to cause ER stress and induce the unfolded protein response (UPR), a process that aims to restore the ER homeostasis by global translation shutdown and increasing the ER folding capacity. The replication of coronavirus, a family of important animal and human pathogens, is closely associated with the cellular membrane compartments, especially the endoplasmic reticulum (ER).