| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T329 |
0-116 |
Sentence |
denotes |
Other interesting signaling pathways included RIG-I-like receptor, PI3K-AKT, mTOR, and autophagy signaling pathways. |
| T330 |
117-703 |
Sentence |
denotes |
As an important family of cytosolic pattern recognition receptors, RIG-I is responsible for sensing of the invading viral RNA by recognizing its pathogen-associated molecular patterns to activate downstream signaling cascades, and thereby produce type I IFN.53,54 The generated IFN molecules then bind to IFN receptors and activate numerous ISGs, which exert critical antiviral innate immune functions either directly or indirectly.55 In our study, five upregulated proteins encoded by ISGs, including ISG15, OAS1, Mx1, IFIT1, and IFIT3, were identified in PDCoV-infected IPEC-J2 cells. |
| T331 |
704-914 |
Sentence |
denotes |
Although these proteins related to type I IFN induction have been reported to participate in diverse viral infections,22,56 most of them were identified for the first time to be associated with PDCoV infection. |
| T332 |
915-1032 |
Sentence |
denotes |
These data suggest that the canonical IFN signaling pathways were activated in IPEC-J2 cells upon infection by PDCoV. |
| T333 |
1033-1415 |
Sentence |
denotes |
This was further confirmed by a recent transcriptome-level study which also demonstrated that the RIG-I-like receptor signaling pathway was activated in PDCoV-infected cells, even though a different type of cells, PK-15, was used.17 Nevertheless, there is increasing evidence suggesting that PDCoV has evolved multiple escape strategies to interfere with the host’s innate immunity. |
| T334 |
1416-2009 |
Sentence |
denotes |
For example, the nsp15 of PDCoV was found to be able to antagonize IFN-β production in LLC-PK1 cells by disrupting the phosphorylation and nuclear translocation of nuclear factor-κB p65 subunit, which is independent of its endoribonuclease activity.57 The Nsp5 of PDCoV was demonstrated to suppress the production of type I IFNs by cleaving the signal transducer and activator of transcription 2, depending on its protease activity.58 Moreover, the PDCoV accessory protein NS6 was shown to antagonize IFN-β production by disrupting the binding of double-stranded RNA to RIG-I/MDA5 receptors.59 |
