ArticleNature communications2022
YAP promotes cell-autonomous immune responses to tackle intracellular Staphylococcus aureus in vitro.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Human airway organoids for bacterial-host interaction studies: methods, insights and translational promise.Thorax · 2026Review
- TNF-α-responsive YAP1 promotes CCL20 expression in colorectal inflammation and cancer.Scientific reports · 2026Article
- Graphene oxide-supported berberine and aloe-emodin nanocomposites for dual-drug release and antimicrobial therapy.Fundamental research · 2026Article
- E3 ubiquitin ligase SKP2 limits autophagosome formation duringFrontiers in cellular and infection microbiology · 2026Article
- Interaction BetweenCurrent pharmaceutical biotechnology · 2026Review
- Harnessing advanced computational approaches to design novel antimicrobial peptides against intracellular bacterial infections.Bioactive materials · 2025Article
- Review
- Strategies for Survival ofInternational journal of molecular sciences · 2025Review
- Evaluation of the penetration capacity of bacteria through layers of different face mask types and wearing conditions.Scientific reports · 2024Article
- Phenol-Soluble Modulin α3 Stimulates Autophagy in HaCaT Keratinocytes.Biomedicines · 2023Article
- The YAP1-TEAD axis promotes autophagy against intracellularAutophagy · 2023Article
- Eliminating the invading extracellular and intracellular FnBpFrontiers in cellular and infection microbiology · 2023Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcriptional cofactors YAP/TAZ have recently been found to support autophagy and inflammation, which are part of cell-autonomous immunity and are critical in antibacterial defense. Here, we studied the role of YAP against Staphylococcus aureus using CRISPR/Cas9-mutated HEK293 cells and a primary cell-based organoid model. We found that S. aureus infection increases YAP transcriptional activity, which is required to reduce intracellular S. aureus replication. A 770-gene targeted transcriptomic analysis revealed that YAP upregulates genes involved in autophagy/lysosome and inflammation pathways in both infected and uninfected conditions. The YAP-TEAD transcriptional activity promotes autophagic flux and lysosomal acidification, which are then important for defense against intracellular S. aureus. Furthermore, the staphylococcal toxin C3 exoenzyme EDIN-B was found effective in preventing YAP-mediated cell-autonomous immune response. This study provides key insights on the anti-S. aureus activity of YAP, which could be conserved for defense against other intracellular bacteria.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.