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[PMID]:29388837
[Au] Autor:Martinez-Jaramillo E; Garza-Morales R; Wechman SL; Montes de Oca-Luna R; Saucedo-Cardenas O; Shirwan H; Yolcu E; McMasters KM; Gomez-Gutierrez JG
[Ad] Endereço:a The Hiram C. Polk Jr., MD, Department of Surgery , University of Louisville School of Medicine , Louisville , USA.
[Ti] Título:Adenovirus Lacking E1b Efficiently Induces Cytopathic Effect in HPV-16-Positive Murine Cancer Cells via Virus Replication and Apoptosis.
[So] Source:Cancer Invest;36(1):19-27, 2018 Jan 02.
[Is] ISSN:1532-4192
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Conditionally replicative adenoviruses (CRAds) replicate poorly in murine cancer cells; however, E1b-deleted CRAds may replicate effectively in HPV16-E6/E7-positive murine cancer cells (TC-1). The HPV16 E7 open reading frame encodes functions analogous to these deleted adenovirus E1 proteins. In this study, an E1b-deleted CRAd (Adhz60) was evaluated for its ability to replicate and induce oncolysis in TC-1 cells. Adhz60-mediated oncolysis was similar in TC-1 and HeLa cells. Productive viral replication was evident based on expression of E1A and hexon, production of infectious virus progeny, and Adhz60-induced apoptosis. The results suggest that TC-1 murine cancer cells allow Adhz60 replication and oncolysis.
[Mh] Termos MeSH primário: Adenoviridae/genética
Proteínas E1B de Adenovirus/genética
Apoptose/genética
Papillomavirus Humano 16/genética
Replicação Viral/genética
[Mh] Termos MeSH secundário: Animais
Apoptose/fisiologia
Linhagem Celular Tumoral
Células HEK293
Células HeLa
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Proteínas Oncogênicas Virais/genética
Proteínas E7 de Papillomavirus/genética
Proteínas Repressoras/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adenovirus E1B Proteins); 0 (E6 protein, Human papillomavirus type 16); 0 (Oncogene Proteins, Viral); 0 (Papillomavirus E7 Proteins); 0 (Repressor Proteins); 0 (oncogene protein E7, Human papillomavirus type 16)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180202
[St] Status:MEDLINE
[do] DOI:10.1080/07357907.2018.1430812


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[PMID]:29331480
[Au] Autor:Xu HH; Zheng LZ; Lin AF; Dong SS; Chai ZY; Yan WH
[Ad] Endereço:Laboratory of Gynecologic Oncology, Medical Research Center, Taizhou Hospital of Zhejiang Province, Wenzhou Medical University, Linhai, Zhejiang, China.
[Ti] Título:Human papillomavirus (HPV) 18 genetic variants and cervical cancer risk in Taizhou area, China.
[So] Source:Gene;647:192-197, 2018 Mar 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Human papillomavirus (HPV) type 18 is predominantly associated with the development of cervical adenocarcinomas, whereas data on HPV18 genetic variability in China are limited. HPV18 genetic variants were formed phylogenetic tree, including lineages A, B, and C. We aimed to evaluate the diversity of HPV18 genetic variants by sequencing the entire E6, E7 and L1 genes. Between 2012 and 2015, a total of 138 (0.8%, 138/17669) women with single HPV18 infection were selected in this study. Finally, we observed 122 HPV18 isolates of the complete E6-E7-L1 sequences, and obtained 36 distinct variation patterns which the accession GenBank numbers as KY457805-KY457840. Except KY457805, KY457813, KY457819, KY457827, KY457829, the rest of HPV18 isolates (81.1%, 31/36) are novel variants. All of HPV18 variants belong to lineage A, while no lineage B, and C was found in our population of Taizhou region, Southeast China. Sublineage A1 was the most common variants (85.2%, 104/122), followed by sublineage A4, A3 and A5, while no sublineage A2 was obtained. Based on the tree topologies, there were three newly identified candidates' sublineages A6-A8. Out of 122 women, 67 (54.9%) had diagnosed by biopsy, including 49 women who diagnosed with cervicitis, 12 with cervical intraepithelial neoplasia (CIN)1, 4 with CIN2/3, and 2 with adenocarcinomas, respectively. Nevertheless, there was no association between HPV18 (sub) lineages and CIN1 or worse (CIN1+) lesions comparing with normal biopsies (P = .469). In conclusion, knowledge of the distribution of geographic/ethnical HPV18 genetic diversity provides critical information for developing diagnostic probes, epidemiologic correlate of cervical cancer risk and design of HPV vaccines for targeted populations.
[Mh] Termos MeSH primário: Variação Genética/genética
Papillomavirus Humano 18/genética
Neoplasias do Colo do Útero/virologia
[Mh] Termos MeSH secundário: Adenocarcinoma/virologia
Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Proteínas do Capsídeo/genética
China
Feminino
Genótipo
Seres Humanos
Meia-Idade
Proteínas Oncogênicas Virais/genética
Proteínas E7 de Papillomavirus/genética
Infecções por Papillomavirus/complicações
Infecções por Papillomavirus/virologia
Risco
Neoplasias do Colo do Útero/etiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Capsid Proteins); 0 (Oncogene Proteins, Viral); 0 (Papillomavirus E7 Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180115
[St] Status:MEDLINE


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[PMID]:28988982
[Au] Autor:Islam S; Mazumder Indra D; Basu M; Roychowdhury A; Das P; Dasgupta H; Roy A; Alam N; Mondal RK; Roychoudhury S; Panda CK
[Ad] Endereço:Department of Oncogene Regulation, Chittaranjan National Cancer Institute, 37, S.P. Mukherjee Road, Kolkata, West Bengal 700026, India.
[Ti] Título:Phylogenetic analysis of Human papillomavirus 16 variants isolated from Indian Breast cancer patients showed difference in genetic diversity with that of cervical cancer isolates.
[So] Source:Virus Res;243:1-9, 2018 01 02.
[Is] ISSN:1872-7492
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The genetic variations of HPV16 in Breast Cancer (BC) are not well studied unlike HPV16 in Cervical Cancer (CACX). In this study, the genetic variations of HPV16 in BC were compared with HPV16 in CACX. In sequencing analysis of LCR, E6 and E7 regions of HPV16 in BC and CACX the A lineage was seen to be 64.2% and 66.6% respectively. The other lineages showed differential frequency in BC and CACX. The mutation frequency index of the regions in BC and CACX was in the following order: LCR>E6>E7. However, the inter-patient genetic diversity in LCR and E6/E7 regions was high in BC than CACX. The LCR region showed more variations than the E6/E7 region in BC. Apart from some common variations, some unique tissue specific variants in LCR and E6/E7 region were seen in BC and in CACX. Besides the selection of some common variants in both BC and CACX, some unique variants in BC (D98Y; 395 G>T) and CACX (R48W; 245 G>T) were observed. The 7521 G>A variant of LCR showed association with Luminal B subtype of BC and progression of CACX. Whereas, 145 G>T (Q14H) and 335 C>T (H78Y) variants of E6 showed association with either early invasiveness of BC and/or poor outcome of the patients. Thus, this study indicates that there may be a difference in the genetic variation of HPV16 in BC and in CACX.
[Mh] Termos MeSH primário: Neoplasias da Mama/virologia
Papillomavirus Humano 16/genética
Papillomavirus Humano 16/isolamento & purificação
Infecções por Papillomavirus/virologia
Filogenia
Neoplasias do Colo do Útero/virologia
[Mh] Termos MeSH secundário: Feminino
Variação Genética
Papillomavirus Humano 16/classificação
Seres Humanos
Índia
Mutação
Proteínas Oncogênicas Virais/genética
Proteínas E7 de Papillomavirus/genética
Proteínas Repressoras/genética
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (E6 protein, Human papillomavirus type 16); 0 (Oncogene Proteins, Viral); 0 (Papillomavirus E7 Proteins); 0 (Repressor Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171010
[St] Status:MEDLINE


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[PMID]:29250535
[Au] Autor:Wang YX; Li YZ; Zhang ZY; Wang JQ; Cui J; Qian XL
[Ad] Endereço:Department of Pathology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang 453003, China.
[Ti] Título:HPV16 E6 Promotes Breast Cancer Proliferation via Upregulation of COX-2 Expression.
[So] Source:Biomed Res Int;2017:2948467, 2017.
[Is] ISSN:2314-6141
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Breast cancer remains the leading cause of cancer-related mortality worldwide. It has been indicated that human papillomaviruses 16 (HPV16) might participate in the pathogenesis and development of breast cancer. However, the detected rate of HPV16 varies with region. We will investigate HPV16 E6 expression in North China and explore the effects and mechanism of HPV16 E6 on breast cancer proliferation in this study. The expressions of HPV16 E6 and COX-2 in paraffin-embedded tissues of the invasive ductal breast cancer were detected by qPCR and IHC. The effects of HPV16 E6 on breast cancer proliferation were determined by function studies. The mechanism of HPV16 E6 in promoting breast cancer proliferation was explored by Western blot and Dual-Luciferase Reporter Assay. HPV16 E6 was positive in 28% invasive ductal breast carcinoma in North China; HPV16 E6 promoted breast cancer proliferation. Inhibition of COX-2 by siCOX-2 or Celecoxib attenuated the proliferation of breast cancer cells with HPV16 E6 expression; and the upregulation of COX-2 could be suppressed by the inhibition of NF- B activity. HPV16 E6 promotes breast cancer proliferation by activation of NF- B signaling pathway and increase of COX-2 expression. COX-2 will be a potential target for HPV16 E6-associated breast cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Neoplasias da Mama/virologia
Proliferação Celular/efeitos dos fármacos
Ciclo-Oxigenase 2/metabolismo
Proteínas Oncogênicas Virais/farmacologia
Proteínas Repressoras/farmacologia
Regulação para Cima/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Feminino
Seres Humanos
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (E6 protein, Human papillomavirus type 16); 0 (Oncogene Proteins, Viral); 0 (Repressor Proteins); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (PTGS2 protein, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1155/2017/2948467


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[PMID]:28463988
[Au] Autor:Calton CM; Bronnimann MP; Manson AR; Li S; Chapman JA; Suarez-Berumen M; Williamson TR; Molugu SK; Bernal RA; Campos SK
[Ad] Endereço:BIO5 Institute, University of Arizona, Tucson, Arizona, United States of America.
[Ti] Título:Translocation of the papillomavirus L2/vDNA complex across the limiting membrane requires the onset of mitosis.
[So] Source:PLoS Pathog;13(5):e1006200, 2017 May.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The human papillomavirus type 16 (HPV16) L2 protein acts as a chaperone to ensure that the viral genome (vDNA) traffics from endosomes to the trans-Golgi network (TGN) and eventually the nucleus, where HPV replication occurs. En route to the nucleus, the L2/vDNA complex must translocate across limiting intracellular membranes. The details of this critical process remain poorly characterized. We have developed a system based on subcellular compartmentalization of the enzyme BirA and its cognate substrate to detect membrane translocation of L2-BirA from incoming virions. We find that L2 translocation requires transport to the TGN and is strictly dependent on entry into mitosis, coinciding with mitotic entry in synchronized cells. Cell cycle arrest causes retention of L2/vDNA at the TGN; only release and progression past G2/M enables translocation across the limiting membrane and subsequent infection. Microscopy of EdU-labeled vDNA reveals a rapid and dramatic shift in vDNA localization during early mitosis. At late G2/early prophase vDNA egresses from the TGN to a pericentriolar location, accumulating there through prometaphase where it begins to associate with condensed chromosomes. By metaphase and throughout anaphase the vDNA is seen bound to the mitotic chromosomes, ensuring distribution into both daughter nuclei. Mutations in a newly defined chromatin binding region of L2 potently blocked translocation, suggesting that translocation is dependent on chromatin binding during prometaphase. This represents the first time a virus has been shown to functionally couple the penetration of limiting membranes to cellular mitosis, explaining in part the tropism of HPV for mitotic basal keratinocytes.
[Mh] Termos MeSH primário: Proteínas do Capsídeo/metabolismo
Genoma Viral/genética
Papillomavirus Humano 16/fisiologia
Mitose
Proteínas Oncogênicas Virais/metabolismo
Infecções por Papillomavirus/virologia
[Mh] Termos MeSH secundário: Transporte Biológico
Proteínas do Capsídeo/genética
Pontos de Checagem do Ciclo Celular
Linhagem Celular
Núcleo Celular/metabolismo
Núcleo Celular/virologia
DNA Viral/genética
DNA Viral/metabolismo
Endossomos/metabolismo
Endossomos/virologia
Papillomavirus Humano 16/genética
Seres Humanos
Queratinócitos/virologia
Mutação
Proteínas Oncogênicas Virais/genética
Tropismo Viral
Vírion
Internalização do Vírus
Rede trans-Golgi/metabolismo
Rede trans-Golgi/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Capsid Proteins); 0 (DNA, Viral); 0 (L2 protein, Human papillomavirus type 16); 0 (Oncogene Proteins, Viral)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006200


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[PMID]:28451790
[Au] Autor:Samuels S; Marijne Heeren A; Zijlmans HJMAA; Welters MJP; van den Berg JH; Philips D; Kvistborg P; Ehsan I; Scholl SME; Nuijen B; Schumacher TNM; van Beurden M; Jordanova ES; Haanen JBAG; van der Burg SH; Kenter GG
[Ad] Endereço:Department of Gynecology, Center for Gynecologic Oncology Amsterdam, P.O. Box 90203, 1006 BE, Amsterdam, The Netherlands.
[Ti] Título:HPV16 E7 DNA tattooing: safety, immunogenicity, and clinical response in patients with HPV-positive vulvar intraepithelial neoplasia.
[So] Source:Cancer Immunol Immunother;66(9):1163-1173, 2017 Sep.
[Is] ISSN:1432-0851
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Usual type vulvar intraepithelial neoplasia (uVIN) is caused by HPV, predominantly type 16. Several forms of HPV immunotherapy have been studied, however, clinical results could be improved. A novel intradermal administration route, termed DNA tattooing, is superior in animal models, and was tested for the first time in humans with a HPV16 E7 DNA vaccine (TTFC-E7SH). METHODS: The trial was designed to test safety, immunogenicity, and clinical response of TTFC-E7SH in twelve HPV16 uVIN patients. Patients received six vaccinations via DNA tattooing. The first six patients received 0.2 mg TTFC-E7SH and the next six 2 mg TTFC-E7SH. Vaccine-specific T-cell immunity was evaluated by IFNγ-ELISPOT and multiparametric flow cytometry. RESULTS: Only grade I-II adverse events were observed upon TTFC-E7SH vaccination. The ELISPOT analysis showed in 4/12 patients a response to the peptide pool containing shuffled E7 peptides. Multiparametric flow cytometry showed low CD4 and/or CD8 T-cell responses as measured by increased expression of PD-1 (4/12 in both), CTLA-4 (2/12 and 3/12), CD107a (5/12 and 4/12), or the production of IFNγ (2/12 and 1/12), IL-2 (3/12 and 4/12), TNFα (2/12 and 1/12), and MIP1ß (3/12 and 6/12). At 3 months follow-up, no clinical response was observed in any of the twelve vaccinated patients. CONCLUSION: DNA tattoo vaccination was shown to be safe. A low vaccine-induced immune response and no clinical response were observed in uVIN patients after TTFC-E7SH DNA tattoo vaccination. Therefore, a new phase I/II trial with an improved DNA vaccine format is currently in development for patients with uVIN.
[Mh] Termos MeSH primário: DNA/genética
Papillomavirus Humano 16/genética
Proteínas Oncogênicas Virais/imunologia
Vacinas de DNA/imunologia
Neoplasias Vulvares/genética
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Meia-Idade
Neoplasias Vulvares/terapia
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Oncogene Proteins, Viral); 0 (Vaccines, DNA); 9007-49-2 (DNA)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1007/s00262-017-2006-y


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[PMID]:27771561
[Au] Autor:Grace M; Munger K
[Ad] Endereço:Department of Developmental, Molecular and Chemical Biology, Tufts University School of Medicine, 150 Harrison Avenue, Jaharis 607, Boston, MA, 02111, USA.
[Ti] Título:Proteomic analysis of the gamma human papillomavirus type 197 E6 and E7 associated cellular proteins.
[So] Source:Virology;500:71-81, 2017 01.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gamma HPV197 was the most frequently identified HPV when human skin cancer specimens were analyzed by deep sequencing (Arroyo Muhr et al., Int. J. Cancer 136: 2546-55, 2015). To gain insight into the biological activities of HPV197, we investigated the cellular interactomes of HPV197 E6 and E7. HPV197 E6 protein interacts with a broad spectrum of cellular LXXLL domain proteins, including UBE3A and MAML1. HPV197 E6 also binds and inhibits the TP53 tumor suppressor and interacts with the CCR4-NOT ubiquitin ligase and deadenylation complex. Despite lacking a canonical retinoblastoma (RB1) tumor suppressor binding site, HPV197 E7 binds RB1 and activates E2F transcription. Hence, HPV197 E6 and E7 proteins interact with a similar set of cellular proteins as E6 and E7 proteins encoded by HPVs that have been linked to human carcinogenesis and/or have transforming activities in vitro.
[Mh] Termos MeSH primário: Gammapapillomavirus/metabolismo
Proteínas Oncogênicas Virais/metabolismo
Proteínas E7 de Papillomavirus/metabolismo
Infecções por Papillomavirus/virologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Gammapapillomavirus/química
Gammapapillomavirus/classificação
Gammapapillomavirus/genética
Seres Humanos
Dados de Sequência Molecular
Proteínas Oncogênicas Virais/química
Proteínas Oncogênicas Virais/genética
Proteínas E7 de Papillomavirus/química
Proteínas E7 de Papillomavirus/genética
Infecções por Papillomavirus/genética
Infecções por Papillomavirus/metabolismo
Ligação Proteica
Proteômica
Alinhamento de Sequência
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Ubiquitina-Proteína Ligases/genética
Ubiquitina-Proteína Ligases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (MAML1 protein, human); 0 (Oncogene Proteins, Viral); 0 (Papillomavirus E7 Proteins); 0 (Transcription Factors); EC 2.3.2.26 (UBE3A protein, human); EC 2.3.2.27 (Ubiquitin-Protein Ligases)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:28464022
[Au] Autor:Aydin I; Villalonga-Planells R; Greune L; Bronnimann MP; Calton CM; Becker M; Lai KY; Campos SK; Schmidt MA; Schelhaas M
[Ad] Endereço:Cellular Virology, Institutes of Molecular Virology and Medical Biochemistry, Center for Molecular Biology of Inflammation (ZMBE), University of Münster, Münster, Germany.
[Ti] Título:A central region in the minor capsid protein of papillomaviruses facilitates viral genome tethering and membrane penetration for mitotic nuclear entry.
[So] Source:PLoS Pathog;13(5):e1006308, 2017 May.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Incoming papillomaviruses (PVs) depend on mitotic nuclear envelope breakdown to gain initial access to the nucleus for viral transcription and replication. In our previous work, we hypothesized that the minor capsid protein L2 of PVs tethers the incoming vDNA to mitotic chromosomes to direct them into the nascent nuclei. To re-evaluate how dynamic L2 recruitment to cellular chromosomes occurs specifically during prometaphase, we developed a quantitative, microscopy-based assay for measuring the degree of chromosome recruitment of L2-EGFP. Analyzing various HPV16 L2 truncation-mutants revealed a central chromosome-binding region (CBR) of 147 amino acids that confers binding to mitotic chromosomes. Specific mutations of conserved motifs (IVAL286AAAA, RR302/5AA, and RTR313EEE) within the CBR interfered with chromosomal binding. Moreover, assembly-competent HPV16 containing the chromosome-binding deficient L2(RTR313EEE) or L2(IVAL286AAAA) were inhibited for infection despite their ability to be transported to intracellular compartments. Since vDNA and L2 were not associated with mitotic chromosomes either, the infectivity was likely impaired by a defect in tethering of the vDNA to mitotic chromosomes. However, L2 mutations that abrogated chromatin association also compromised translocation of L2 across membranes of intracellular organelles. Thus, chromatin recruitment of L2 may in itself be a requirement for successful penetration of the limiting membrane thereby linking both processes mechanistically. Furthermore, we demonstrate that the association of L2 with mitotic chromosomes is conserved among the alpha, beta, gamma, and iota genera of Papillomaviridae. However, different binding patterns point to a certain variance amongst the different genera. Overall, our data suggest a common strategy among various PVs, in which a central region of L2 mediates tethering of vDNA to mitotic chromosomes during cell division thereby coordinating membrane translocation and delivery to daughter nuclei.
[Mh] Termos MeSH primário: Proteínas do Capsídeo/metabolismo
Genoma Viral/genética
Papillomavirus Humano 16/genética
Mitose
Proteínas Oncogênicas Virais/metabolismo
[Mh] Termos MeSH secundário: Transporte Biológico
Proteínas do Capsídeo/genética
Núcleo Celular/metabolismo
Núcleo Celular/virologia
Cromatina/genética
Cromossomos/genética
DNA Viral/genética
DNA Viral/metabolismo
Genes Reporter
Papillomavirus Humano 16/fisiologia
Seres Humanos
Membranas Intracelulares/metabolismo
Membranas Intracelulares/virologia
Mutação
Proteínas Oncogênicas Virais/genética
Vírion
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Capsid Proteins); 0 (Chromatin); 0 (DNA, Viral); 0 (L2 protein, Human papillomavirus type 16); 0 (Oncogene Proteins, Viral)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006308


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[PMID]:28448850
[Au] Autor:Harden ME; Munger K
[Ad] Endereço:Program in Virology, Division of Medical Sciences, Harvard Medical School Boston, MA 02115, USA; Department of Developmental, Molecular and Chemical Biology, Tufts University School of Medicine, Boston, MA 02111, USA.
[Ti] Título:Perturbation of DROSHA and DICER expression by human papillomavirus 16 oncoproteins.
[So] Source:Virology;507:192-198, 2017 07.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Many tumors, including cervical carcinoma, show dysregulated expression of the microRNA processing machinery, specifically DROSHA and DICER. Some cervical cancers exhibit chromosome 5p amplifications and DROSHA is the most significantly upregulated transcript and is observed in all tumors with 5p gain. DROSHA and DICER mRNA levels, however, are higher in HPV positive cancer lines than in an HPV negative cervical carcinoma line. We show that high-risk HPV E6/E7 expression in HPV negative C33A cervical carcinoma cells and primary human epithelial cell causes increased expression of DROSHA and DICER mRNA and protein. Most importantly, many DROSHA regulated microRNAs are dysregulated in HPV16 E6/E7 expressing cells. These results suggest that increased DROSHA levels contribute to HPV16 E6/E7 dysregulation of cellular microRNA expression.
[Mh] Termos MeSH primário: RNA Helicases DEAD-box/genética
Papillomavirus Humano 16/metabolismo
Proteínas Oncogênicas Virais/metabolismo
Proteínas E7 de Papillomavirus/metabolismo
Infecções por Papillomavirus/genética
Proteínas Repressoras/metabolismo
Ribonuclease III/genética
Neoplasias do Colo do Útero/genética
[Mh] Termos MeSH secundário: RNA Helicases DEAD-box/metabolismo
Feminino
Regulação Neoplásica da Expressão Gênica
Papillomavirus Humano 16/genética
Seres Humanos
MicroRNAs/genética
MicroRNAs/metabolismo
Proteínas Oncogênicas Virais/genética
Proteínas E7 de Papillomavirus/genética
Infecções por Papillomavirus/metabolismo
Infecções por Papillomavirus/virologia
Proteínas Repressoras/genética
Ribonuclease III/metabolismo
Neoplasias do Colo do Útero/metabolismo
Neoplasias do Colo do Útero/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (E6 protein, Human papillomavirus type 16); 0 (MicroRNAs); 0 (Oncogene Proteins, Viral); 0 (Papillomavirus E7 Proteins); 0 (Repressor Proteins); 0 (oncogene protein E7, Human papillomavirus type 16); EC 3.1.26.3 (DICER1 protein, human); EC 3.1.26.3 (DROSHA protein, human); EC 3.1.26.3 (Ribonuclease III); EC 3.6.4.13 (DEAD-box RNA Helicases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171220
[Lr] Data última revisão:
171220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE


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[PMID]:29023483
[Au] Autor:Xu WX; Wang J; Tang HP; Chen LH; Lian WB; Zhan JM; Gupta SK; Ji CN; Gu SH; Xie Y
[Ad] Endereço:Division of Reproductive Immunology, Key Lab of Reproduction Regulation of NPFPC, Shanghai Institute of Planned Parenthood Research, Fudan University, Shanghai, P. R. China.
[Ti] Título:A simpler and more cost-effective peptide biosynthetic method using the truncated GST as carrier for epitope mapping.
[So] Source:PLoS One;12(10):e0186097, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There is a need to develop better methods for epitope mapping and/or identification of antibody-recognizing motifs. Here, we describe improved biosynthetic peptide (BSP) method using a newly developed plasmid pXXGST-3 as vector, which has a viral E7 gene in the cloning sites of pXXGST-1. It is crucial to employ pXXGST-3 instead of pXXGST-1, since it makes use of the BSP method simpler and easier to perform, and more cost-effective for epitope mapping. These merits are embodied in two aspects: i) convenient recovery of double enzyme-digested product due to the existence of 315 bp inserted between BamH I and Sal I sites, and thus greatly reducing the production of self-ligation clones, and ii) no longer requiring control protein when screening recombinant (r-) clones expressing 8/18mer peptides by running polyacrylamide gel electrophoresis. The protocol involves the following core steps: (i) design of plus and minus strands of DNA fragments encoding overlapping 8/18mer peptides; (ii) chemical synthesis of the designed DNA fragments; (iii) development of r-clones using pXXGST-3 vector expressing each 8/18mer peptide fused with truncated GST188 protein; (iv) screening r-clones by running the cell pellets from each induced clone on SDS-PAGE gel followed by sequencing of inserted DNA fragments for each verified r-clone; and (v) Western blotting with either monoclonal antibodies or polyclonal antibodies. This improved GST188-BSP method provides a powerful alternative tool for epitope mapping.
[Mh] Termos MeSH primário: Mapeamento de Epitopos/métodos
Glutationa Transferase/metabolismo
Peptídeos/metabolismo
Plasmídeos/genética
Engenharia de Proteínas/métodos
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/metabolismo
Mapeamento de Epitopos/economia
Glutationa Transferase/genética
Imunização
Masculino
Proteínas Oncogênicas Virais/genética
Peptídeos/imunologia
Engenharia de Proteínas/economia
Coelhos
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Oncogene Proteins, Viral); 0 (Peptides); 0 (Recombinant Fusion Proteins); EC 2.5.1.18 (Glutathione Transferase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186097



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