English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Significance The cap structure present at the 5′ end of eukaryotic messenger RNAs (mRNAs) regulates RNA stability, translation, and marks mRNA as self, thereby impeding recognition by the innate immune system. Cellular transcripts beginning with adenosine are additionally modified at the N6 position of the 2’-O methylated cap-proximal residue by the methyltransferase PCIF1 to m7 Gpppm6 Am . We define a function for this N6-adenosine methylation in attenuating the interferon-β–mediated suppression of viral infection. Cells lacking PCIF1, or defective in its enzymatic activity, augment the cell-intrinsic suppressive effect of interferon-β treatment on vesicular stomatitis virus (VSV) and rabies virus (RABV) gene expression. VSV and RABV mRNAs are efficiently methylated by PCIF1, suggesting this contributes to viral evasion of innate immune suppression.

Methylation of viral mRNA cap structures by PCIF1 attenuates the antiviral activity of interferon-β