PML isoforms IV and V contribute to adenovirus-mediated oncogenic transformation by functionally inhibiting the tumor-suppressor p53

Oncogene
Peter WimmerSabrina Schreiner

Abstract

Although modulation of the cellular tumor-suppressor p53 is considered to have the major role in E1A/E1B-55K-mediated tumorigenesis, other promyelocytic leukemia nuclear body (PML-NB)/PML oncogenic domain (POD)-associated factors including SUMO, Mre11, Daxx, as well as the integrity of these nuclear bodies contribute to the transformation process. However, the biochemical consequences and oncogenic alterations of PML-associated E1B-55K by SUMO-dependent PML-IV and PML-V interaction have so far remained elusive. We performed mutational analysis to define a PML interaction motif within the E1B-55K polypeptide. Our results showed that E1B-55K/PML binding is not required for p53, Mre11 and Daxx interaction. We also observed that E1B-55K lacking subnuclear PML localization because of either PML-IV or PML-V-binding deficiency was no longer capable of mediating E1B-55K-dependent SUMOylation of p53, inhibition of p53-mediated transactivation or efficiently transforming primary rodent cells. These results together with the observation that E1B-55K-dependent SUMOylation of p53 is required for efficient cell transformation, provides evidence for the idea that the SUMO ligase activity of the E1B-55K viral oncoprotein is intimately linked t...Continue Reading

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Citations

Nov 6, 2015·Journal of Virology·Carolin BürckSabrina Schreiner
Sep 22, 2016·MBio·Sook-Young Sohn, Patrick Hearing
Jan 13, 2017·Journal of Molecular Cell Biology·Ban Xiong TanCynthia R Coffill
Nov 27, 2019·FEBS Letters·Paloma HidalgoRamón A Gonzalez
Sep 8, 2015·Viruses·Peter Wimmer, Sabrina Schreiner
Jan 6, 2021·Cells·Neerajana DattaMrinal K Ghosh
Dec 29, 2020·Virus Research·Samuel HofmannSabrina Schreiner
Feb 17, 2021·Médecine sciences : M/S·Justine DespresKarim Benihoud

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