ArticleOncogene2003
UVB irradiation reduces the half-life and transactivation potential of the human papillomavirus 16 E2 protein.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Human papillomavirus 16 E2 blocks cellular senescence in response to activation of the DNA damage response.Virology · 2022Article
- Interaction with TopBP1 Is Required for Human Papillomavirus 16 E2 Plasmid Segregation/Retention Function during Mitosis.Journal of virology · 2022Article
- Article
- Human Papillomavirus E2 Regulates SRSF3 (SRp20) To Promote Capsid Protein Expression in Infected Differentiated Keratinocytes.Journal of virology · 2016Article
- Regulation of human genome expression and RNA splicing by human papillomavirus 16 E2 protein.Virology · 2014Article
- The papillomavirus E2 proteins.Virology · 2013Review
- Equine sarcoids: Bovine Papillomavirus type 1 transformed fibroblasts are sensitive to cisplatin and UVB induced apoptosis and show aberrant expression of p53.Veterinary research · 2012Article
- Sunspot dynamics are reflected in human physiology and pathophysiology.Astrobiology · 2011Article
- Runx regulation of sphingolipid metabolism and survival signaling.Cancer research · 2010Article
- RNA splicing factors regulated by HPV16 during cervical tumour progression.The Journal of pathology · 2009Article
- TopBP1 regulates human papillomavirus type 16 E2 interaction with chromatin.Journal of virology · 2007Article
- TopBP1 contains a transcriptional activation domain suppressed by two adjacent BRCT domains.The Biochemical journal · 2006Article
- SF2/ASF binds the human papillomavirus type 16 late RNA control element and is regulated during differentiation of virus-infected epithelial cells.Journal of virology · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human papillomaviruses (HPV) are causative agents of human cancers including those of the cervix and also of the head and neck; HPV16 is the most commonly found type in these diseases. The viral E2 protein regulates transcription from the viral genome by interacting with DNA-binding sequences in the HPV transcriptional control region; it also regulates replication by interacting with and recruiting the HPV replication factor E1 to the viral origin. Therefore, E2 is essential for the viral life cycle. The E2 protein interacts with several proteins involved in the cellular response to DNA damage including p53, TopBP1, and PARP. We therefore set out to establish whether DNA-damaging agents can regulate E2 activity. Here we show that UVB irradiation downregulates transcriptional activity of both HPV16 and HPV8 E2, while hydroxyurea and etoposide do not. This downregulation of E2 activity is independent of p53 function as it occurs in p53 wild type and null cell types as well as in the presence of functional HPV16 E6 that degrades p53. Using stable cell lines expressing E2 we show that this downregulation of E2 function by UVB is due to a reduction of the E2 protein half-life. The identification of the pathway(s) through which UVB downregulates E2 transcriptional activity and protein levels will present a novel target for the treatment of HPV-related diseases.
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Registered trials
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