Adenovirus E1A binding to DCAF10 targets proteasomal degradation of RUVBL1/2 AAA+ ATPases required for quaternary assembly of multiprotein machines, innate immunity, and responses to metabolic stress.

Autor:	Zemke NR; Molecular Biology Institute, University of California, Los Angeles, California, USA.; Department of Cellular and Molecular Medicine, UCSD School of Medicine, La Jolla, California, USA.; Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, California, USA., Hsu E; Molecular Biology Institute, University of California, Los Angeles, California, USA.; Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, California, USA.; Department of Biological Chemistry, David Geffen School of Medicine at UCLA, Los Angeles, California, USA., Barshop WD; Thermo Fisher Scientific, San Jose, California, USA.; Department of Biochemistry and Molecular Medicine and the Norris Comprehensive Cancer Center, Keck School of Medicine, USC, Los Angeles, California, USA., Sha J; Thermo Fisher Scientific, San Jose, California, USA., Wohlschlegel JA; Molecular Biology Institute, University of California, Los Angeles, California, USA.; Thermo Fisher Scientific, San Jose, California, USA., Berk AJ; Molecular Biology Institute, University of California, Los Angeles, California, USA.; Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, California, USA.
Jazyk:	angličtina
Zdroj:	Journal of virology [J Virol] 2023 Dec 21; Vol. 97 (12), pp. e0099323. Date of Electronic Publication: 2023 Nov 14.
DOI:	10.1128/jvi.00993-23
Abstrakt:	Importance: Inactivation of EP300/CREBB paralogous cellular lysine acetyltransferases (KATs) during the early phase of infection is a consistent feature of DNA viruses. The cell responds by stabilizing transcription factor IRF3 which activates transcription of scores of interferon-stimulated genes (ISGs), inhibiting viral replication. Human respiratory adenoviruses counter this by assembling a CUL4-based ubiquitin ligase complex that polyubiquitinylates RUVBL1 and 2 inducing their proteasomal degradation. This inhibits accumulation of active IRF3 and the expression of anti-viral ISGs, allowing replication of the respiratory HAdVs in the face of inhibition of EP300/CBEBBP KAT activity by the N-terminal region of E1A. Competing Interests: The authors declare no conflict of interest.
Databáze:	MEDLINE
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