ArticleJournal of virology2001
Stability of the human papillomavirus type 18 E2 protein is regulated by a proteasome degradation pathway through its amino-terminal transactivation domain.
Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 55 citations in OpenAlex.
- Preclinical Immunogenicity and Efficacy Studies for Therapeutic Vaccines for Human Papillomavirus-Type-16-Associated Cancer.Vaccines · 2024Article
- Regulation of the Human Papillomavirus Lifecyle through Post-Translational Modifications of the Viral E2 Protein.Pathogens (Basel, Switzerland) · 2021Review
- Cyclic AMP-Dependent Protein Kinase Exhibits Antagonistic Effects on the Replication Efficiency of Different Human Papillomavirus Types.Journal of virology · 2021Article
- The CXCL12/CXCR4 Signaling Pathway: A New Susceptibility Factor in Human Papillomavirus Pathogenesis.PLoS pathogens · 2016Article
- The role of ubiquitin and ubiquitin-like modification systems in papillomavirus biology.Viruses · 2014Review
- Brd4-mediated nuclear retention of the papillomavirus E2 protein contributes to its stabilization in host cells.Viruses · 2014Article
- E2 proteins of high risk human papillomaviruses down-modulate STING and IFN-κ transcription in keratinocytes.PloS one · 2014Article
- CCHCR1 interacts specifically with the E2 protein of human papillomavirus type 16 on a surface overlapping BRD4 binding.PloS one · 2014Article
- The papillomavirus E2 proteins.Virology · 2013Review
- Using bleach-chase to measure protein half-lives in living cells.Nature protocols · 2012Article
- The HPV E2-Host Protein-Protein Interactions: A Complex Hijacking of the Cellular Network.The open virology journal · 2012Article
- Large scale genotype comparison of human papillomavirus E2-host interaction networks provides new insights for e2 molecular functions.PLoS pathogens · 2012Article
- Loss of HPV16 E2 Protein Expression Without Disruption of the E2 ORF Correlates with Carcinogenic Progression.The open virology journal · 2012Article
- NRIP, a novel calmodulin binding protein, activates calcineurin to dephosphorylate human papillomavirus E2 protein.Journal of virology · 2011Article
- The human papillomavirus type 18 E2 protein is a cell cycle-dependent target of the SCFSkp2 ubiquitin ligase.Journal of virology · 2010Article
- Brd4 regulation of papillomavirus protein E2 stability.Journal of virology · 2009Article
- Ubiquitination, ubiquitin-like modifiers, and deubiquitination in viral infection.Cell host & microbe · 2009Review
- Proteasomal degradation of the papillomavirus E2 protein is inhibited by overexpression of bromodomain-containing protein 4.Journal of virology · 2009Article
- Article
- Tax1BP1 interacts with papillomavirus E2 and regulates E2-dependent transcription and stability.Journal of virology · 2009Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The E2 proteins of papillomaviruses regulate both viral transcription and DNA replication. The human papillomavirus type 18 (HPV18) E2 protein has been shown to repress transcription of the oncogenic E6 and E7 genes, inducing growth arrest in HeLa cells. Using HPV18 E2 fused to the green fluorescent protein (GFP), we showed that this protein was short-lived in transfected HeLa cells. Real-time microscopy experiments indicated that the E2-dependent signal increased for roughly 24 h after transfection and then rapidly disappeared, indicating that E2 was unstable in HeLa cells and could confer instability to GFP. Similar studies done with a protein lacking the transactivation domain indicated that this truncation strongly stabilizes the E2 protein. In vitro, full-length E2 or the transactivation domain alone was efficiently ubiquitinated, whereas deletion of the transactivation domain strongly decreased the ubiquitination of the E2 protein. Proteasome inhibition in cells expressing E2 increased its half-life about sevenfold, which was comparable to the half-life of the amino-terminally truncated protein. These characteristics of E2 instability were independent of the E2-mediated G(1) growth arrest in HeLa cells, as they were reproduced in MCF7 cells, where E2 does not affect the cell cycle. Altogether, these experiments showed that the HPV18 E2 protein was degraded by the ubiquitin-proteasome pathway through its amino-terminal transactivation domain. Tight regulation of the stability of the HPV 18 E2 protein may be essential to avoid accumulation of a potent transcriptional repressor and antiproliferative agent during the viral vegetative cycle.
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