@article{fdi:010077737,
  title = {{T}he {RNA} binding protein {Q}uaking represses host interferon response by downregulating {MAVS}},
  author = {{L}iao, {K}. {C}. and {C}huo, {V}. and {F}agg, {W}. {S}. and {B}radrick, {S}. {S}. and {P}ompon, {J}ulien and {G}arcia-{B}lanco, {M}. {A}.},
  editor = {},
  language = {{ENG}},
  abstract = {{Q}uaking ({QKI}) is an {RNA}-binding protein ({RBP}) involved in multiple aspects of {RNA} metabolism and many biological processes. {D}espite a known immune function in regulating monocyte differentiation and inflammatory responses, the degree to which {QKI} regulates the host interferon ({IFN}) response remains poorly characterized. {H}ere we show that {QKI} ablation enhances poly({I}:{C}) and viral infection-induced {IFN} beta transcription. {C}haracterization of {IFN}-related signalling cascades reveals that {QKI} knockout results in higher levels of {IRF}3 phosphorylation. {I}nterestingly, complementation with {QKI}-5 isoform alone is sufficient to rescue this phenotype and reduce {IRF}3 phosphorylation. {F}urther analysis shows that {MAVS}, but not {RIG}-{I} or {MDA}5, is robustly upregulated in the absence of {QKI}, suggesting that {QKI} downregulates {MAVS} and thus represses the host {IFN} response. {A}s expected, {MAVS} depletion reduces {IFN} beta activation and knockout of {MAVS} in the {QKI} knockout cells completely abolishes {IFN} beta induction. {C}onsistently, ectopic expression of {RIG}-{I} activates stronger {IFN} beta induction via {MAVS}-{IRF}3 pathway in the absence of {QKI}. {C}ollectively, these findings demonstrate a novel role for {QKI} in negatively regulating host {IFN} response by reducing {MAVS} levels.},
  keywords = {{QKI} ; {IFN} ; {IRF}3 ; {MAVS} ; viral infection},
  booktitle = {},
  journal = {{RNA} {B}iology},
  volume = {17},
  numero = {3},
  pages = {366--380},
  ISSN = {1547-6286},
  year = {2020},
  DOI = {10.1080/15476286.2019.1703069},
  URL = {https://www.documentation.ird.fr/hor/fdi:010077737},
}