TRIM23 prevents adenovirus replication by p62-mediated selective autophagic degradation of viral E1A protein.

Authors

Nan Sun, Jikai Zhang, Banruo Xia, Hang Yin, Jiaqian Xie, Xiaoxiao Liu, Man Li, Lin Fang, Guijuan Ji, Gaolei Ma, Haihan Zhang, Zhenzhen Wang, Dafei Chai, Gang Wang

Published in

PLoS pathogens. Volume 22. Issue 9. Pages e1014578. Sep 08, 2026. Epub Sep 08, 2026.

Abstract

The E3 ubiquitin ligase TRIM23 is involved in diverse cellular processes, however, its function in antiviral defense against adenovirus remains unclear. Here, we identify a novel mechanism by which TRIM23 restricts human adenovirus type 5 (HAdV-C5) replication. TRIM23 expression was upregulated upon HAdV-C5 infection, and functional studies showed that its overexpression inhibited viral replication, while knockdown enhanced it. Mechanistically, TRIM23 interacts with the viral E1A protein and promotes its degradation through a mechanism dependent of its canonical E3 ligase activity. Moreover, TRIM23 recruits the selective autophagy receptor p62 promotes E1A degradation in a E1A ubiquitination-independent manner. Our results unveil a novel host defense pathway-the TRIM23-E1A-p62 axis-that highlights the role of selective autophagy in antiviral immunity.

PMID:
42709852
Bibliographic data and abstract were imported from PubMed on 09 Sep 2026.

Read full publication at:
Please sign in to see all details.

Stats

1-terrible, 9-excellent. How would you rate this publication? Sign in in to submit your rating.

Post a comment

You need to be signed in to post comments. You can sign in here.

Comments

There are no comments yet.