Littérature scientifique sur le sujet « HPV16 E7 »
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Articles de revues sur le sujet "HPV16 E7"
Alsanea, Madain, Asma Alsaleh, Dalia Obeid, Faten Alhadeq, Basma Alahideb et Fatimah Alhamlan. « Genetic Variability in the E6, E7, and L1 Genes of Human Papillomavirus Types 16 and 18 among Women in Saudi Arabia ». Viruses 15, no 1 (30 décembre 2022) : 109. http://dx.doi.org/10.3390/v15010109.
Texte intégralGiarrè, Marianna, Sandra Caldeira, Ilaria Malanchi, Francesca Ciccolini, Maria João Leão et Massimo Tommasino. « Induction of pRb Degradation by the Human Papillomavirus Type 16 E7 Protein Is Essential To Efficiently Overcome p16INK4a-Imposed G1 Cell Cycle Arrest ». Journal of Virology 75, no 10 (15 mai 2001) : 4705–12. http://dx.doi.org/10.1128/jvi.75.10.4705-4712.2001.
Texte intégralMa, Yunyan, LV Xiaoyan, Xiaojiang Jia, Jingzhen Zhou, Zhenbo Ouyang, Zhen Gao, Wenjuan Qiao, Xin Liu et Ninghu Zhu. « The Role and Mechanism of Human Papillomavirus16 E7 (HPV16 E7) in the Proliferation and Invasion of Cervical Cancer Cells Through Regulating Forkhead Box Protein A1 ». Journal of Biomaterials and Tissue Engineering 10, no 8 (1 août 2020) : 1206–12. http://dx.doi.org/10.1166/jbt.2020.2481.
Texte intégralWulandari, Dwi, Lisnawati Rachmadi et Tjahjani M. Sudiro. « Phylogenetic analysis and predicted functional effect of protein mutations of E6 and E7 HPV16 strains isolated in Indonesia ». Medical Journal of Indonesia 24, no 4 (31 décembre 2015) : 197–205. http://dx.doi.org/10.13181/mji.v24i4.1197.
Texte intégralNguyen, Christine L., et Karl Münger. « Human Papillomavirus E7 Protein Deregulates Mitosis via an Association with Nuclear Mitotic Apparatus Protein 1 ». Journal of Virology 83, no 4 (3 décembre 2008) : 1700–1707. http://dx.doi.org/10.1128/jvi.01971-08.
Texte intégralSantin, Alessandro D., Stefania Bellone, Michela Palmieri, Alessandro Zanolini, Antonella Ravaggi, Eric R. Siegel, Juan J. Roman, Sergio Pecorelli et Martin J. Cannon. « Human Papillomavirus Type 16 and 18 E7-Pulsed Dendritic Cell Vaccination of Stage IB or IIA Cervical Cancer Patients : a Phase I Escalating-Dose Trial ». Journal of Virology 82, no 4 (5 décembre 2007) : 1968–79. http://dx.doi.org/10.1128/jvi.02343-07.
Texte intégralNguyen, Christine L., Catherine Eichwald, Max L. Nibert et Karl Münger. « Human Papillomavirus Type 16 E7 Oncoprotein Associates with the Centrosomal Component γ-Tubulin ». Journal of Virology 81, no 24 (3 octobre 2007) : 13533–43. http://dx.doi.org/10.1128/jvi.01669-07.
Texte intégralZhou, Fang, JieZhong Chen et Kong-Nan Zhao. « Human papillomavirus 16-encoded E7 protein inhibits IFN-γ-mediated MHC class I antigen presentation and CTL-induced lysis by blocking IRF-1 expression in mouse keratinocytes ». Journal of General Virology 94, no 11 (1 novembre 2013) : 2504–14. http://dx.doi.org/10.1099/vir.0.054486-0.
Texte intégralHayashi, Shigenori, Takashi Iwata, Ryotaro Imagawa, Masaki Sugawara, Guanliang Chen, Satoko Tanimoto, Yo Sugawara et al. « Transcription Factor Homeobox D9 Drives the Malignant Phenotype of HPV18-Positive Cervical Cancer Cells via Binding to the Viral Early Promoter ». Cancers 13, no 18 (15 septembre 2021) : 4613. http://dx.doi.org/10.3390/cancers13184613.
Texte intégralHuh, KyungWon, Xiaobo Zhou, Hiroyuki Hayakawa, Je-Yoel Cho, Towia A. Libermann, Jianping Jin, J. Wade Harper et Karl Munger. « Human Papillomavirus Type 16 E7 Oncoprotein Associates with the Cullin 2 Ubiquitin Ligase Complex, Which Contributes to Degradation of the Retinoblastoma Tumor Suppressor ». Journal of Virology 81, no 18 (3 juillet 2007) : 9737–47. http://dx.doi.org/10.1128/jvi.00881-07.
Texte intégralThèses sur le sujet "HPV16 E7"
Ruiz, Elena. « DNA fusion vaccines against HPV16 E7 antigen-associated cancers ». Thesis, University of Southampton, 2011. https://eprints.soton.ac.uk/374745/.
Texte intégralEberhard, Jeremy. « Studies on the Nucleocytoplasmic Transport of the E7 Oncoprotein of High-Risk HPV Type 16 ». Thesis, Boston College, 2013. http://hdl.handle.net/2345/3293.
Texte intégralHuman papillomaviruses (HPVs) have been estimated to be the most common sexually transmitted infection in the United States. In addition to condyloma accuminata, infection of the squamous basal epithelium by high-risk HPVs, notably type 16 (HPV16), has been shown to be the primary etiological agent in the majority of cervical carcinomas. The E7 major transforming protein of HPV16, along with E6, has been linked to tumorigenesis and malignancy. While the E7 protein itself possesses no enzymatic activity, its ability to bind a number of nuclear and cytoplasmic targets subverts a variety of cellular regulatory complexes and facilitates viral replication. Previous studies in the Moroianu Lab have shown the HPV16 E7 oncoprotein to translocate across the nuclear pore complex (NPC) in a facilitated manner dependent on a non-canonical, c-terminal, nuclear localization signal (cNLS) for import, and a consensus leucine-rich nuclear export sequence (NES) for export (28). While the leucine-rich NES has been characterized, a full examination of the cNLS has yet to be performed. Here we present evidence that the karyopherin independent nuclear import mediated by the cNLS of 16E7 is dependent on its c-terminal Zn binding domain. Furthermore, we demonstrate that nuclear import is mediated by the direct interaction of a small patch of hydrophobic residues, 65LRLCV69, with the FG domain of the central FG-nucleoporin Nup62. In addition, we examined a potential regulatory mechanism of 16E7 nucleocytoplasmic translocation. Previous work has shown that a serine conserved in the high-risk HPVs at position 71 is phosphorylated by an unknown kinase. Here we present evidence that while phosphorylation of S71 is not required for either 16E7 nuclear localization or nuclear export in HeLa cells, mimicking phosphorylation of the S71 residue results in a statistically significant shift in the distribution of localization phenotypes of the resultant cell population toward a larger percentage exhibiting more nuclear localization. These data suggest that nucleocytoplasmic transport of 16E7 is, at least in part, a regulated process
Thesis (PhD) — Boston College, 2013
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Biology
Nicol, Clare. « Selection and characterisation of RNA aptamers to the human papillomavirus 16 (HPV16) E7 oncoprotein ». Thesis, University of Leeds, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.535664.
Texte intégralSoares, Alexandra Sabrina Antunes. « Purification of HPV16 E6/E7 DNA plasmid-based vaccine using a modified monolithic support ». Master's thesis, Universidade da Beira Interior, 2013. http://hdl.handle.net/10400.6/1344.
Texte intégralO Papiloma Vírus Humano é um vírus sexualmente transmissível que está relacionado com o desenvolvimento de vários cancros, como o cancro do colo do útero. Este tipo de cancro é a segunda maior causa de morte em mulheres, afetando mundialmente cerca de meio milhão de mulheres, das quais aproximadamente 274 mil morrem. A evidente associação que existe entre o Papiloma Vírus Humano e o cancro do colo do útero torna o Papiloma Vírus Humano um alvo interessante para o desenvolvimento de vacinas, no sentido de prevenir ou tratar o desenvolvimento do cancro. Atualmente, já são comercializadas duas vacinas preventivas, a Gardasil da Merck e a Cervarix da GlaxoSmithKline. Apesar de ambas mostrarem ser eficazes e seguras, possuem algumas limitações como elevado custo, não protegem contra todos os tipos de Papiloma Vírus Humano e trata-se de vacinas exclusivamente preventivas. Assim o desenvolvimento de vacinas terapêuticas pode ser uma estratégia promissora para colmatar estas falhas. A utilização do DNA plasmídico (pDNA) como uma vacina não viral tem-se tornado numa potencial estratégia terapêutica para prevenir ou tratar determinadas doenças de forma menos invasiva e segura comparando com os vetores virais. O mecanismo de actuação desta vacina baseia-se na expressão de proteínas antigénicas que desencadeiam uma resposta imunológica, evitando a progressão da doença . A preparação destas vacinas de DNA plasmídico requer o desenvolvimento de processos de produção e purificação que permitam obter grandes quantidades de plasmídeo na sua forma biologicamente ativa (isoforma superenrolada (sc)), cumprindo os requisitos das agências reguladoras no que diz respeito ao grau de pureza. Da ocorrência natural de complexos proteínas-DNA em sistemas biológicos sugeriu o desenvolvimento de uma estratégia de cromatografia de afinidade, utilizando matrizes convencionais de agarose com determinados aminoácidos imobilizados que reconhecem especificamente a isoforma superenrolada do DNA plasmídico. No entanto, as matrizes convencionais apresentam algumas limitações quando comparadas com os suportes monolíticos que possuem excelentes propriedades de transferência de massa e elevada capacidade de ligação para moléculas de grandes dimensões como o DNA plasmídico. Desta forma, o trabalho apresentado nesta tese consistiu na modificação de um monolito de epoxy por imobilização de aminoácidos de arginina, conjugando assim a selectividade deste ligando com a versatilidade do monolito de epoxy, tendo como finalidade purificar a isoforma sc do pDNA HPV-16 E6/E7. Numa fase inicial, foram realizados vários ensaios com amostras de DNA plasmídico pre-purificadas com o kit comercial, no sentido de avaliar e confirmar a presença dos ligandos de arginina, comparando o comportamento cromatográfico do monolito modificado com o mesmo suporte não modificado. Os resultados comprovaram que o monolito modificado reconhece especialmente o DNA plasmídico, permitindo a separação das isoformas superenrolada e circular aberta através de um gradiente por passos de NaCl. O mesmo não aconteceu com o monolito de epoxy não modificado, pois não ocorreu qualquer tipo de interacção do plasmídeo com o suporte. Posteriormente foi realizado um estudo de capacidade de ligação dinâmica para completar a caracterização do monolito com ligandos de arginina e comparar com a coluna convencional de arginina-argarose. Os resultados comprovaram que, para as mesmas condições de caudal e concentração de pDNA HPV-16 E6/E7, o monolito possui uma capacidade de ligação significativamente superior em comparação com a coluna convencional. Uma vez conseguida a separação das isoformas e a caracterização do monolito modificado com a arginina, a segunda fase do trabalho consistiu na purificação da isoforma sc do pDNA HPV-16 E6/E7 a partir de um lisado complexo de Escherichia coli. Os testes de controlo de qualidade revelaram que a amostra de sc de pDNA HPV-16 E6/E7, resultante da purificação com o monolito de epoxy modificado, apresentava um grau de pureza de aproximadamente 100% e uma homogeneidade superior a 97%. Para além disso, constituintes do hospedeiro como RNA e proteínas não foram detectados na amostra purificada e a quantidade de DNA genómico e endotoxinas estavam a baixo dos valores referenciados pelas agências reguladoras como a Food and Drug Delivery. Em suma, a combinação de ligandos de aminoácidos com suportes monolíticos pode ser uma solução promissora para obtenção de uma vacina não-viral baseada na isoforma sc do pDNA HPV-16 E6/E7, com o grau de pureza requerido para futuras aplicações terapêuticas contra a infecção por Papiloma Vírus Humano.
D'ANNA-BEAUGIE, ROSSELLA. « Etude des effets de l'onco-proteine virale hpv16-e7 sur les cellules endotheliales humaines ». Paris 6, 2001. http://www.theses.fr/2001PA066257.
Texte intégralKo, Kevin. « Investigation of the Interactions Between the DREAM Complex and HPV16 ». VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5786.
Texte intégralMorale, Mirian Galliote. « Desenvolvimento de vacina terapêutica contra HPV16 ». Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-26042010-160643/.
Texte intégralCervical cancer is the second most common cancer among women worldwide. Most cases (83%) occur in developing countries, where they are found in relatively advanced stages and, consequently, the median survival is about 49% after five years. Therefore, an effective vaccine against HPV infections can lead to control of cancer of the cervix. Although preventable, the prophylactic HPV vaccine is not accessible to all due to their high cost and in addition the vaccine does not eliminate the HPV in infected women. We have therefore proposed the development of effective therapeutic vaccines using two approaches: chimeric VLPs (virus-like particles), endowed with prophylactic and therapeutic properties, obtained from the fusion protein L1 and E7; chimeric proteins derived from the fusion of epitopes of proteins E6 and E7 of HPV16 with and without ubiquitin. After subcloning, we obtained the vectors pPICHOLI-L1ΔCE71-50 and L1 pPICHOLI- L1ΔCE743-77. After transformation of yeast Pichia pastoris with these constructions, the cells were induced, but it was not possible to detect any recombinant protein expression. As an alternative, we proposed the expression of synthetic proteins in E. coli derived from the fusion between epitopes of E6 and E7 proteins of HPV16 with or without Ubiquitin, in order to enhance the presentation of peptides through MHC class I to stimulate the elimination of HPV16-infected cells, preventing and regressing the development of cancer cells. Soluble E6E7 protein was purified and, 20% of the animals immunized with this protein did not develop tumor after inoculation of TC1 cells. In a second immunization experiment we compared the proteins E6E7 and E6E7Ub, in two concentrations, 15 and 40µg, with or without the adjuvant whole cell pertussis (WCP). Regardless of concentration and presence or absence of WCP, all the groups immunized with E6E7Ub showed protection against tumor between 80% and 100%, while the groups immunized with E6E7 showed protection from 0% to 25%. These results are promising and although preliminary, indicate the potential of E6E7Ub protein as an immunogen, for a therapeutic vaccine against cervical cancer induced by HPV16
MARZANO, VALERIA. « Indagine di proteomica su linee cellulari polmonari umane stabilmente infettate con gli oncogeni E6 ed E7 di HPV16 ». Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2008. http://hdl.handle.net/2108/435.
Texte intégralIn recent years data have accumulated implicating the involvement of oncogenic HPVs in bronchial carcinogenesis and the presence and expression of oncogenic HPV transcripts in non-small cell lung cancers have been reported throughout distinct studies. Taken together these data seem to support the hypothesis that oncogenic HPVs could act as co-factor in lung carcinogenesis. To further understand the role of HPV in the development of lung cancer we employed the lung cell line A549 stably infected with HPV16E6, HPV16E7 and HPV16E6/E7 constructs to investigate by a proteomic approach the protein profile changes associated with the expression of these oncogenes. Replicated 2-DE gels from uninfected and stably HPV16E6/E7 infected A549 cells were compared for changes in protein profile. We identified 17 different polypeptides whose average normalized spot intensity was statistically significant (p<0.05) and differed by 2- fold. The protein identification was achieved by peptide mass fingerprinting by MALDI-TOF-MS and nLC-ESI-Q-TOF-MS/MS peptide ladder sequencing Relationships between differentially expressed proteins and the HPV-induced infection mechanism have been clustered by knowledge-base database functional association network analysis. The results, deriving from the networks obtained from all three different infection conditions, suggested the functional involvement of a cell death inhibition pathway with central nodes including Annexin IV, Gp96, Hsp27 and Tumor protein-translationally controlled 1 as major key proteins for cell viability and inhibition of apoptosis pathway.
Kavati, Erica Akemi. « Interação de oncoproteínas virais E6 e E7 de HPV16/18 com alvos celulares potenciais para o desenvolvimento de estratégias terapêuticas ». Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/87/87131/tde-26112012-103224/.
Texte intégralThe oncogenic potential of HPV is based on the capacity of viral oncoproteins E6 and E7 to change cellular cycle leading to immortality and malignancy. The important role of oncoproteins in tumor progression and its interaction with numerous cellular targets have relevance in studies to the development of vaccines and therapies against HPV associated cancers. This study investigated intracellular localization of E6 and E7 HPV16/18 oncoproteins and its possible cellular targets. It showed the presence of E6 in the cellular nucleus, cytoplasm, and intramitochondrial in naturally HPV transformed cell, as well as in cells transfected with E6 viral oncogene. E7 was detected inside nucleus and cytoplasm, but E7 intramitochondrial did not occur. This study confirmed the hypothesis of the intramitochondrial presence of E6 viral oncoprotein from high risk HPV. This is an original data whose relevance is directly related to clinical application in the development of immunobiologicals and drugs, which are able to neutralize the action of this important therapeutic target.
Giannouli, Christina. « Evaluation pré-clinique de vaccins contre le cancer du col utérin basés sur la vaccination avec des protéines E7 de HPV16 recombinantes ». Doctoral thesis, Universite Libre de Bruxelles, 2002. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/211393.
Texte intégralChapitres de livres sur le sujet "HPV16 E7"
Phelps, W. C., C. L. Yee, K. Münger et P. M. Howley. « Functional and Sequence Similarities Between HPV16 E7 and Adenovirus E1A ». Dans Transforming Proteins of DNA Tumor Viruses, 153–66. Berlin, Heidelberg : Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74578-2_19.
Texte intégralLondoño, Patricia, Robert Tindle, Ian Frazer, Steve Chatfield et Gordon Dougan. « Use of Double Aro Salmonella Mutants to Stably Express HPV16 E7 Protein Epitopes Carried by HBV Core Antigen ». Dans Immunology of Human Papillomaviruses, 299–303. Boston, MA : Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2449-6_46.
Texte intégralLiu, Xiang, Yongwei Lai, Hailin Yao, Mengmeng Zhang, Hao Zhou, Tongcun Zhang et Hongpeng He. « HPV18 E6 and E7 Influence the Expression of Cancer Related LncRNAs in HeLa Cells ». Dans Lecture Notes in Electrical Engineering, 719–27. Singapore : Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4801-2_74.
Texte intégralFeltkamp, Mariet C. W., Michel P. M. Vierboom, Jan ter Schegget, Cornelis J. M. Melief et W. Martin Kast. « Fine Characterization of the HPVI6 E7 49-57 Tumor Protective Cytotoxic T Cell Epitope “Rahynivtf” ». Dans Immunology of Human Papillomaviruses, 275–81. Boston, MA : Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2449-6_43.
Texte intégralActes de conférences sur le sujet "HPV16 E7"
Jadaun, Alka, Sourabh Prakash et Saurabh Gupta. « Identification of Novel Inhibitors Against HPV16/18-E7 for Cancer Therapy ». Dans 2018 International Conference on Bioinformatics and Systems Biology (BSB). IEEE, 2018. http://dx.doi.org/10.1109/bsb.2018.8770694.
Texte intégralAgarwal, Maria, Ashley Saint-Fleur, Jie Fu, Hyam Levitsky et Cornelia L. Trimble. « Abstract 4048 : HPV16 immunity induced by immune responses to mutations in E6 and E7 proteins ». Dans Proceedings : AACR 106th Annual Meeting 2015 ; April 18-22, 2015 ; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4048.
Texte intégralAbboodi, Fadi F., Kim E. Creek et Lucia A. Pirisi. « Abstract LB-329 : Molecular mechanisms of loss of E7 expression in HPV16-transformed human keratinocytes ». Dans Proceedings : AACR Annual Meeting 2019 ; March 29-April 3, 2019 ; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-lb-329.
Texte intégralMcGhee, Eva, Mengtao Li, Yi-Ling Lin, Khadijah Lang, Meidrah Tyler, Judith Okoro, Mai Do et al. « Abstract 3789 : Genomic instability changes acquired by HPV16 E6/E7 targeting multipolar mitoses aneuploidy : Cellular sequelae ». Dans Proceedings : AACR Annual Meeting 2019 ; March 29-April 3, 2019 ; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3789.
Texte intégralMcGhee, Eva, Mengtao Li, Yi-Ling Lin, Khadijah Lang, Meidrah Tyler, Judith Okoro, Mai Do et al. « Abstract 3789 : Genomic instability changes acquired by HPV16 E6/E7 targeting multipolar mitoses aneuploidy : Cellular sequelae ». Dans Proceedings : AACR Annual Meeting 2019 ; March 29-April 3, 2019 ; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3789.
Texte intégralJian, Z. « 29 E6-P53 AND E7-RB co-mediated higher carcinogenic ability of HPV16 than HPV58 in cervical cancer ». Dans IGCS Annual 2019 Meeting Abstracts. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/ijgc-2019-igcs.29.
Texte intégralMcGhee, Eva, Mengtao Li, Yi-Ling Lin, Liliana Zarate, Naomi Long, Mai Do, Chinelo Ezechukwu et al. « Abstract 3326 : Upregulation of epigenetic changes acquired by HPV16 E6/E7 oncoproteins in mouse keratinocytes : Targeting ATM/PI3K ». Dans Proceedings : AACR Annual Meeting 2018 ; April 14-18, 2018 ; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3326.
Texte intégralGosmann, Christina, Stephen R. Mattarollo, Antje Blumenthal et Ian H. Frazer. « Abstract A47 : Increased levels of IL-12, IL-23 and IL-18 in skin expressing HPV16 E7 protein. » Dans Abstracts : AACR Special Conference on Tumor Immunology : Multidisciplinary Science Driving Basic and Clinical Advances ; December 2-5, 2012 ; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-a47.
Texte intégralGrunwitz, C., V. Jahndel, J. Braun, D. Schwarck-Kokarakis, F. Vascotto, J. Setzer, E. King, CH Ottensmeier, Ö. Türeci et U. Sahin. « PO-516 E6/E7 RNA(LIP) : a novel liposomal RNA vaccine for treatment of patients with HPV16-positive malignancies ». Dans Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.531.
Texte intégralChung, Christine, Dimitrios Colevas, Douglas Adkins, Jong Chul Park, Cristina Rodriguez, Michael Gibson, Ammar Sukari et al. « 681 A phase 1 study of CUE-101, a novel HPV16 E7-pHLA-IL2-Fc fusion protein, as monotherapy and in combination with pembrolizumab in patients with recurrent/metastatic HPV16+ head and neck cancer ». Dans SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0681.
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