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• W2891995078 abstract "Th2 immune response is critical for allergic asthma pathogenesis. Molecular mechanisms for regulating Th2 immunity are still not well understood. Here we report that the ubiquitin-specific protease USP38 is crucial for Th2-mediated allergic asthma. TCR stimulation up-regulated the USP38 level, and USP38 in turn mediated the protein stabilization of JunB, a transcription factor specific for Th2 development. Consequently, USP38 was specifically required for TCR-induced production of Th2 cytokines and Th2 development both in vitro and in vivo, and USP38-deficient mice were resistant to asthma pathogenesis induced by OVA or HDM. Mechanistically, USP38 directly associated with JunB, deubiquitinated Lys-48–linked poly-ubiquitination of JunB, and consequently blocked TCR-induced JunB turnover. USP38 represents the first identified deubiquitinase specifically for Th2 immunity and the associated asthma." @default.
• W2891995078 created "2018-09-27" @default.
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• W2891995078 date "2018-09-17" @default.
• W2891995078 modified "2023-10-13" @default.
• W2891995078 title "USP38 critically promotes asthmatic pathogenesis by stabilizing JunB protein" @default.
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• W2891995078 doi "https://doi.org/10.1084/jem.20172026" @default.
• W2891995078 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6219735" @default.
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