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DDX56 inhibits PRV replication through regulation of IFN-β signaling pathway by targeting cGAS - PMC
Source: ncbi.nlm.nih.gov
Article summary:
1. DDX56 has the ability to inhibit PRV replication in vitro, which may be an important factor for PRV infection.
2. DDX56 exerts its proliferation-inhibitory effects of PRV through up-regulating cGAS-STING-induced IFN-β expression.
3. DDX56 plays a promotion role in IRF3 phosphorylation and nucleus translocation, providing insight into host control of PRV proliferation.
Article analysis:
The article is generally reliable and trustworthy, as it provides evidence for its claims and presents both sides of the argument equally. The authors provide evidence for their claims by demonstrating that overexpression of DDX56 inhibited PRV genomic DNA transcription and lower titers of PRV infection in PK15 cells, whereas down-regulation of the DDX56 expression had a promotion role on virus replication. Furthermore, they demonstrate that DDX56 could promote cGAS expression and direct interaction also existed between DDX56 and cGAS. Additionally, they show that knockdown of cGAS expression could abrogate the inhibition role of DDX56 on PRV proliferation and weaken the effect of DDX56 on IFN-β expression. The article does not appear to have any biases or one-sided reporting, as it presents both sides of the argument equally. It does not appear to have any unsupported claims or missing points of consideration either; all claims are supported by evidence provided in the article. There is no promotional content or partiality present in the article either; it is purely scientific in nature. The article does note possible risks associated with its findings, such as potential implications for human health if PRV poses a risk to humans as indicated by some cases with clinical signs. All in all, this article appears to be reliable and trustworthy overall.