ArticleJournal of virology1997
A papillomavirus E2 phosphorylation mutant exhibits normal transient replication and transcription but is defective in transformation and plasmid retention.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Regulation of the Human Papillomavirus Lifecyle through Post-Translational Modifications of the Viral E2 Protein.Pathogens (Basel, Switzerland) · 2021Review
- Human Papillomavirus 31 Tyrosine 102 Regulates Interaction with E2 Binding Partners and Episomal Maintenance.Journal of virology · 2020Article
- The papillomavirus E2 proteins.Virology · 2013Review
- Acetylation of conserved lysines in bovine papillomavirus E2 by p300.Journal of virology · 2013Article
- Replication and transcription of human papillomavirus type 58 genome in Saccharomyces cerevisiae.Virology journal · 2010Article
- Topography of bovine papillomavirus E2 protein on the viral genome during the cell cycle.Virology · 2009Article
- Tax1BP1 interacts with papillomavirus E2 and regulates E2-dependent transcription and stability.Journal of virology · 2009Article
- Characterization of the functional activities of the bovine papillomavirus type 1 E2 protein single-chain heterodimers.Journal of virology · 2006Article
- Regulation of the EBNA1 Epstein-Barr virus protein by serine phosphorylation and arginine methylation.Journal of virology · 2006Article
- High-throughput screening of the yeast kinome: identification of human serine/threonine protein kinases that phosphorylate the hepatitis C virus NS5A protein.Journal of virology · 2004Article
- E1 protein of bovine papillomavirus type 1 interferes with E2 protein-mediated tethering of the viral DNA to mitotic chromosomes.Journal of virology · 2002Article
- Stability of the human papillomavirus type 18 E2 protein is regulated by a proteasome degradation pathway through its amino-terminal transactivation domain.Journal of virology · 2001Article
- Reconstitution of Epstein-Barr virus-based plasmid partitioning in budding yeast.The EMBO journal · 2001Article
- Proteasome-mediated degradation of the papillomavirus E2-TA protein is regulated by phosphorylation and can modulate viral genome copy number.Journal of virology · 2000Article
- The E8E2C protein, a negative regulator of viral transcription and replication, is required for extrachromosomal maintenance of human papillomavirus type 31 in keratinocytes.Journal of virology · 2000Article
- Alleviation of human papillomavirus E2-mediated transcriptional repression via formation of a TATA binding protein (or TFIID)-TFIIB-RNA polymerase II-TFIIF preinitiation complex.Molecular and cellular biology · 2000Article
- Stability without a centromere.Proceedings of the National Academy of Sciences of the United States of America · 1998Review
- Segregation of viral plasmids depends on tethering to chromosomes and is regulated by phosphorylation.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Competition for DNA binding sites between the short and long forms of E2 dimers underlies repression in bovine papillomavirus type 1 DNA replication control.Journal of virology · 1998Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Papillomavirus DNA persists in infected cells as a nuclear plasmid, causing epithelial lesions in many hosts, including humans. The viral protein E2 is required for both replication and transcription to facilitate this persistence. Bovine papillomavirus E2 protein is phosphorylated at two predominant sites. Phosphorylation of one of these sites (serine 301) inhibits replication of the genome. Using mass spectrometry and Edman sequencing, we have mapped additional phosphorylation sites in tryptic peptides to positions which lie primarily in the putatively unstructured hinge region of E2. Mutation of the major sites facilitates transformation in the absence of viral repressors and only has a minor effect on transformation when the repressors are present. Mutation of the major phosphorylation sites combined with one additional change at a newly discovered site (serine 235) blocks transformation. Transformation can be restored by mutating this residue to aspartic acid, mimicking a phosphorylated amino acid, suggesting that phosphorylation is key to the regulation. Transformation by the mutant genome can also be rescued by ectopic expression of the E2 enhancer protein, demonstrating a loss of function by the mutant protein and not a toxic defect. In transient assays, phosphorylation site mutants of E2 protein were normal for all viral functions tested, including replication, transcriptional activation and repression (by the overlapping mutant repressors), protein accumulation, and surprisingly, viral oncogene E5 promoter activation. While the mutant genome transiently replicated to high levels, stable replication was defective, suggesting that a function of E2 required for plasmid retention is regulated by phosphorylation.
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