ArticleVirology2011
A cyclin-binding motif in human papillomavirus type 18 (HPV18) E1^E4 is necessary for association with CDK-cyclin complexes and G2/M cell cycle arrest of keratinocytes, but is not required for differentiation-dependent viral genome amplification or L1 capsid protein expression.
Article in Virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- Manipulation of the cell cycle by HIV-1.Biochemical Society transactions · 2026Review
- Repression of CADM1 transcription by HPV type 18 is mediated by three-dimensional rearrangement of promoter-enhancer interactions.PLoS pathogens · 2025Article
- The potential use of therapeutics and prophylactic mRNA vaccines in human papillomavirus (HPV).Virology journal · 2024Review
- Exploitation of ATP-sensitive potassium ion (KOncogene · 2023Article
- Downregulation of Sonic hedgehog signaling induces G2-arrest in genital warts.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2023Article
- Senolytic Therapy: A Potential Approach for the Elimination of Oncogene-Induced Senescent HPV-Positive Cells.International journal of molecular sciences · 2022Review
- E6-mediated activation of JNK drives EGFR signalling to promote proliferation and viral oncoprotein expression in cervical cancer.Cell death and differentiation · 2021Article
- Article
- Modelling human papillomavirus biology in oropharyngeal keratinocytes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Review
- STAT3 activation by E6 is essential for the differentiation-dependent HPV18 life cycle.PLoS pathogens · 2018Article
- Article
- Mitotic control of human papillomavirus genome-containing cells is regulated by the function of the PDZ-binding motif of the E6 oncoprotein.Oncotarget · 2017Article
- Article
- Synthetic lethal mutations in the cyclin A interface of human cytomegalovirus.PLoS pathogens · 2017Article
- Genomic characterization of a novel Epsilonpapillomavirus associated with pigmented papillomas in a red deer (Cervus elaphus).Virus genes · 2016Article
- Evidence of disrupted high-risk human papillomavirus DNA in morphologically normal cervices of older women.Scientific reports · 2016Article
- Modulation of therapeutic sensitivity by human papillomavirus.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2015Review
- The human papillomavirus (HPV) E7 protein antagonises an Imiquimod-induced inflammatory pathway in primary human keratinocytes.Scientific reports · 2015Article
- CCCTC-binding factor recruitment to the early region of the human papillomavirus 18 genome regulates viral oncogene expression.Journal of virology · 2015Article
- Human papillomavirus type 1 E1^E4 protein is a potent inhibitor of the serine-arginine (SR) protein kinase SRPK1 and inhibits phosphorylation of host SR proteins and of the viral transcription and replication regulator E2.Journal of virology · 2014Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The G2/M arrest function of human papillomavirus (HPV) E4 proteins is hypothesized to be necessary for viral genome amplification. Full-length HPV18 E1^E4 protein is essential for efficient viral genome amplification. Here we identify key determinants within a CDK-bipartite consensus recognition motif in HPV18 E1^E4 that are critical for association with active CDK-cyclin complexes and in vitro phosphorylation at the predicted CDK phosphorylation site (threonine 23). The optimal cyclin-binding sequence ((43)RRLL(46)) within this E4 motif is required for G2/M arrest of primary keratinocytes and correlates with cytoplasmic retention of cyclin B1, but not cyclin A. Disruption of this motif in the E4 ORF of HPV18 genomes, and the subsequent generation of stable cell lines in primary keratinocytes revealed that this motif was not essential for viral genome amplification or L1 capsid protein induction. We conclude that the HPV18 E4 G2/M arrest function does not play a role in early vegetative events.
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