1998
Transactivation-Competent Bovine Papillomavirus E2 Protein Is Specifically Required for Efficient Repression of Human Papillomavirus Oncogene Expression and for Acute Growth Inhibition of Cervical Carcinoma Cell Lines
Goodwin E, Naeger L, Breiding D, Androphy E, DiMaio D. Transactivation-Competent Bovine Papillomavirus E2 Protein Is Specifically Required for Efficient Repression of Human Papillomavirus Oncogene Expression and for Acute Growth Inhibition of Cervical Carcinoma Cell Lines. Journal Of Virology 1998, 72: 3925-3934. PMID: 9557678, PMCID: PMC109618, DOI: 10.1128/jvi.72.5.3925-3934.1998.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBinding SitesBovine papillomavirus 1CattleCell DivisionCell NucleusCOS CellsDNADNA-Binding ProteinsFemaleGene Expression Regulation, ViralHeLa CellsHumansMutagenesisOncogene Proteins, ViralOncogenesPapillomaviridaeRepressor ProteinsRNA, MessengerRNA, ViralTrans-ActivatorsTranscriptional ActivationTumor Cells, CulturedUterine Cervical NeoplasmsViral ProteinsConceptsPapillomavirus E2 proteinGrowth arrestHT-3 cellsEfficient repressionTransactivation domainE2 proteinHeLa cellsG1/S-phase growth arrestE2 mutantsBovine papillomavirus type 1 E2 proteinBovine papillomavirus E2 proteinHerpes simplex virus VP16Reporter plasmidAcute growth inhibitionE2 transactivation domainGrowth inhibitionCervical carcinoma cell linesBPV1 E2 proteinCarcinoma cell linesHuman papillomavirus oncogene expressionViral DNA replicationPhase growth arrestSequence-specific transactivatorCell linesWild-type p53 gene
1990
Integrated HPV 1 genomes in a human keratinocyte cell line can be transactivated by a SV40/BPV1 recombinant virus which expresses BPV1 E2 proteins
Partow A, Grand R, Biggs P, Jeffrey S, Dimaio D, Gallimore P. Integrated HPV 1 genomes in a human keratinocyte cell line can be transactivated by a SV40/BPV1 recombinant virus which expresses BPV1 E2 proteins. Virology 1990, 175: 508-517. PMID: 2158183, DOI: 10.1016/0042-6822(90)90435-t.Peer-Reviewed Original ResearchCell Line, TransformedClone CellsDNA, RecombinantDNA, ViralDNA-Binding ProteinsGene Expression Regulation, ViralHumansKaryotypingKeratinocytesNucleic Acid HybridizationPapillomaviridaePolymerase Chain ReactionRecombinant ProteinsRNA SplicingSimian virus 40Transcription, GeneticTranscriptional ActivationTransfectionViral ProteinsBovine papillomavirus E2 repressor mutant displays a high-copy-number phenotype and enhanced transforming activity
Riese D, Settleman J, Neary K, DiMaio D. Bovine papillomavirus E2 repressor mutant displays a high-copy-number phenotype and enhanced transforming activity. Journal Of Virology 1990, 64: 944-949. PMID: 2153255, PMCID: PMC249196, DOI: 10.1128/jvi.64.2.944-949.1990.Peer-Reviewed Original ResearchConceptsRepressor proteinWild-type copy numberBovine papillomavirus type 1 genomeCopy numberViral genomeTranscriptional repressor proteinTransient expression experimentsMouse C127 cellsMutant viral DNAViral DNAType 1 genomeNumber phenotypeRepressor activityLow copy numberMethionine codonInitiation codonExpression experimentsC127 cellsGenomeCV1 cellsRepressor mutantsFoci formationColony formationCodonProtein
1989
Genetic evidence that acute morphologic transformation, induction of cellular DNA synthesis, and focus formation are mediated by a single activity of the bovine papillomavirus E5 protein.
Settleman J, Fazeli A, Malicki J, Horwitz B, DiMaio D. Genetic evidence that acute morphologic transformation, induction of cellular DNA synthesis, and focus formation are mediated by a single activity of the bovine papillomavirus E5 protein. Molecular And Cellular Biology 1989, 9: 5563-5572. PMID: 2555701, PMCID: PMC363726, DOI: 10.1128/mcb.9.12.5563.Peer-Reviewed Original ResearchConceptsE5 proteinE5 geneCellular DNA synthesisC127 cellsBovine papillomavirus E5 proteinMouse C127 cellsDNA synthesisMorphologic transformationCultured rodent cellsDefective phenotypeMissense mutantsUnstable proteinDefective mutantsGenetic evidenceMutational analysisE5 activityRodent cellsCell cycleViral genesBiochemical activitySerum starvationCell transformationGenesContact inhibitionVirus multiplicity