ArticleeLife2025
SARS-CoV-2 NSP13 interacts with TEAD to suppress Hippo-YAP signaling.
Article in eLife, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Recent advances in functional studies of coronavirus NSP13 helicase and challenges in inhibitor development.Virulence · 2026Review
- SARS-CoV-2 Nsp13 helicase resolves G-quadruplexes and is inhibited by G4 ligands or an antiviral regulator: Implications for G4 anti-coronavirus therapies.The Journal of biological chemistry · 2026Article
- Hippo signalling as a nexus in host-virus interactions.PLoS pathogens · 2026Review
- Bacterial Effector Screening Reveals RNF214 as a Virus Restriction Factor in Mammals.bioRxiv : the preprint server for biology · 2024Article
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12 authors.
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Abstract
The Hippo pathway controls organ development, homeostasis, and regeneration primarily by modulating YAP/TEAD-mediated gene expression. Although emerging studies report Hippo-YAP dysfunction after viral infection, it is largely unknown in the context of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Here, we analyzed RNA sequencing data from human-induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) and SARS-CoV-2-infected human lung samples, and observed a decrease in YAP target gene expression. In screening SARS-CoV-2 nonstructural proteins, we found that nonstructural protein 13 (NSP13), a conserved coronavirus helicase, inhibits YAP transcriptional activity independent of the upstream Hippo kinases LATS1/2. Consistently, introducing NSP13 into mouse cardiomyocytes suppresses an active form of YAP (YAP5SA)
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