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Comment
. 2018 Jun;15(6):642-644.
doi: 10.1038/cmi.2017.97. Epub 2017 Oct 23.

Relief of YAP-mediated inhibition by IKKɛ promotes innate antiviral immunity

Nayoung Kim  1   2 , Yun-Yong Park  3   4 , Chul Hyun Joo  5 , Hun Sik Kim  6   7
Affiliations
Comment

Relief of YAP-mediated inhibition by IKKɛ promotes innate antiviral immunity

Nayoung Kim et al. Cell Mol Immunol. 2018 Jun.
No abstract available

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
YAP regulates innate antiviral immunity via a transcription-independent mechanism. YAP/TAZ are major effectors of the Hippo pathway and are involved in organ size control and tissue homeostasis in normal cells. However, when dysregulated, they act as oncoproteins and promote cellular responses that are associated with tumor initiation, growth and metastasis. In general, these functions require the interaction of YAP/TAZ with TEAD family transcription factors (TEAD1–4) and thus rely on transcription-dependent mechanism. Now, Wang et al. have identified a transcription-independent function of YAP as a negative regulator of innate antiviral immunity. YAP4, a transcriptionally inactive isoform, also blocks the activation of IRF3 at the dimerization step and thus limits IFN-β expression in response to viral nucleic acids. Notably, IKKɛ that is activated by viral infection induces lysosomal degradation of YAP via phosphorylation at Ser403 and thereby relieves the YAP-mediated suppression of IRF3. Thus, YAP is likely a new physiologic regulator of innate antiviral immunity and a potential therapeutic target for the modulation of IFN-β expression.
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