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USP38 critically promotes asthmatic pathogenesis by stabilizing JunB protein.

A new interesting article has been published in J Exp Med. 2018 Nov 5;215(11):2850-2867. doi: 10.1084/jem.20172026. Epub 2018 Sep 17. and titled:

USP38 critically promotes asthmatic pathogenesis by stabilizing JunB protein.

Authors of this article are:

Chen S, Yun F, Yao Y, Cao M, Zhang Y, Wang J, Song X, Qian Y.

A summary of the article is shown below:

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.

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