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| Content Provider | PubMed Central |
|---|---|
| Author | Cho, Jin A. Lee, Ann-hwee Platzer, Barbara Cross, Benedict C. S. Gardner, Brooke M. Luca, Heidi De Luong, Phi Harding, Heather P. Glimcher, Laurie H. Walter, Peter Fiebiger, Edda Ron, David Kagan, Jonathan C. Lencer, Wayne I. |
| Copyright Year | 2013 |
| Abstract | The plasma membrane and all membrane-bound organelles except for the Golgi and endoplasmic reticulum (ER) are equipped with pattern-recognition molecules to sense microbes or their products and induce innate immunity for host defense. Here, we report that inositol-requiring-1α (IRE1α), an ER protein that signals in the unfolded protein response (UPR), is activated to induce inflammation by binding a portion of cholera toxin as it co-opts the ER to cause disease. Other known UPR transducers, including the IRE1α-dependent transcription factor XBP1, are dispensable for this signaling. The inflammatory response depends instead on the RNase activity of IRE1α to degrade endogenous mRNA, a process termed regulated IRE1α-dependent decay (RIDD) of mRNA. The mRNA fragments produced engage retinoic-acid inducible gene 1 (RIG-I), a cyto-solic sensor of RNA viruses, to activate NF-κB and interferon pathways. We propose IRE1α provides for a generalized mechanism of innate immune surveillance originating within the ER lumen. |
| Related Links | http://dx.doi.org/10.1016/j.chom.2013.03.011 |
| Ending Page | 569 |
| Page Count | 12 |
| Starting Page | 558 |
| File Format | |
| ISSN | 19346069 |
| e-ISSN | 19346069 |
| Journal | Cell host & microbe |
| Issue Number | 5 |
| Volume Number | 13 |
| Language | English |
| Publisher Date | 2013-05-15 |
| Access Restriction | Open |
| Subject Keyword | Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Virology Parasitology Microbiology |
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