ArticleBMC molecular biology2012
A point mutation in the DNA-binding domain of HPV-2 E2 protein increases its DNA-binding capacity and reverses its transcriptional regulatory activity on the viral early promoter.
Article in BMC molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Genetic Variability and Prediction of T Epitopes of the HPV16 E2 Gene in Asymptomatic Women from Cajamarca, Peru.Viruses · 2025Article
- Structural and functional roles of conserved residues of human papillomavirus (HPV) E2 protein and biological consequences.Virology journal · 2025Article
- In Silico Identification of Potential Antagonists Targeting the HPV16 E2-E1 Interaction: A Step Toward Novel Therapeutics for Cervical Cancer.Current issues in molecular biology · 2025Article
- L-type association between magnesium intake and human papillomavirus infection in US adult women: based on NHANES 2003-2016 data.Frontiers in nutrition · 2025Article
- Article
- Physics-Based Potentials for Coarse-Grained Modeling of Protein-DNA Interactions.Journal of chemical theory and computation · 2015Article
- Sequence variation in the E2-binding domain of HPV16 and biological function evaluation in Tunisian cervical cancers.BioMed research international · 2014Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe human papillomavirus (HPV) E2 protein is a multifunctional DNA-binding protein. The transcriptional activity of HPV E2 is mediated by binding to its specific binding sites in the upstream regulatory region of the HPV genomes. Previously we reported a HPV-2 variant from a verrucae vulgaris patient with huge extensive clustered cutaneous, which have five point mutations in its E2 ORF, L118S, S235P, Y287H, S293R and A338V. Under the control of HPV-2 LCR, co-expression of the mutated HPV E2 induced an increased activity on the viral early promoter. In the present study, a series of mammalian expression plasmids encoding E2 proteins with one to five amino acid (aa) substitutions for these mutations were constructed and transfected into HeLa, C33A and SiHa cells.
resultsCAT expression assays indicated that the enhanced promoter activity was due to the co-expressions of the E2 constructs containing A338V mutation within the DNA-binding domain. Western blots analysis demonstrated that the transiently transfected E2 expressing plasmids, regardless of prototype or the A338V mutant, were continuously expressed in the cells. To study the effect of E2 mutations on its DNA-binding activity, a serial of recombinant E2 proteins with various lengths were expressed and purified. Electrophoresis mobility shift assays (EMSA) showed that the binding affinity of E2 protein with A338V mutation to both an artificial probe with two E2 binding sites or HPV-2 and HPV-16 promoter-proximal LCR sequences were significantly stronger than that of the HPV-2 prototype E2. Furthermore, co-expression of the construct containing A338V mutant exhibited increased activities on heterologous HPV-16 early promoter P97 than that of prototype E2.
conclusionsThese results suggest that the mutation from Ala to Val at aa 338 is critical for E2 DNA-binding and its transcriptional regulation.
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