Gotowe bibliografie tematyczne / HPV-18 LCR

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  1. Artykuły w czasopismach
  2. Rozprawy doktorskie

Gotowa bibliografia na temat „HPV-18 LCR”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 9 lutego 2022

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Artykuły w czasopismach na temat "HPV-18 LCR"

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Wyant, Patrícia Soares, Daniela Marreco Cerqueira, Daniella Sousa Moraes, José Paulo Gagliardi Leite, Cláudia Renata Fernandes Martins, Marcelo de Macedo Brígido, and Tainá Raiol. "Phylogeny and Polymorphism in the Long Control Region, E6, and L1 of Human Papillomavirus Types 53, 56, and 66 in Central Brazil." International Journal of Gynecologic Cancer 21, no. 2 (January 2011): 222–29. http://dx.doi.org/10.1097/igc.0b013e318208c73d.

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Introduction:Several studies related that different human papillomavirus (HPV) types and intratype variants can present different oncogenic potential. In opposite to HPVs 16 and 18 variants, information about variants of other carcinogenic HPV types is still scarce. The aim of this study was to investigate the genetic variability of HPVs 53, 56, and 66 from Central Brazil isolates.Methods:The long control region (LCR), E6, and L1 genomic regions were amplified and sequenced. We evaluate for nucleotide variations in relation to the reference sequence of each HPV type and also the conservation o
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Stünkel, Walter, and Hans-Ulrich Bernard. "The Chromatin Structure of the Long Control Region of Human Papillomavirus Type 16 Represses Viral Oncoprotein Expression." Journal of Virology 73, no. 3 (March 1, 1999): 1918–30. http://dx.doi.org/10.1128/jvi.73.3.1918-1930.1999.

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ABSTRACT The long control region (LCR) of human papillomavirus type 16 (HPV-16) has a size of 850 bp (about 12% of the viral genome) and regulates transcription and replication of the viral DNA. The 5′ segment of the LCR contains transcription termination signals and a nuclear matrix attachment region, the central segment contains an epithelial cell-specific enhancer, and the 3′ segment contains the replication origin and the E6 promoter. Here we report observations on the chromatin organization of this part of the HPV-16 genome. Treatment of the nuclei of CaSki cells, a cell line with 500 int
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Díaz-Tejeda, Yakelin, Miriam C. Guido-Jiménez, Helga López-Carbajal, Alfredo Amador-Molina, Rocío Méndez-Martínez, Patricio Gariglio-Vidal, Marcela Lizano, and Alejandro García-Carrancá. "Nanog, in Cooperation with AP1, Increases the Expression of E6/E7 Oncogenes from HPV Types 16/18." Viruses 13, no. 8 (July 28, 2021): 1482. http://dx.doi.org/10.3390/v13081482.

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Persistent infections with some types of human papillomavirus (HPV) constitute the major etiological factor for cervical cancer development. Nanog, a stem cell transcription factor has been shown to increase during cancer progression. We wanted to determine whether Nanog could modulate transcription of E6 and E7 oncogenes. We used luciferase reporters under the regulation of the long control region (LCR) of HPV types 16 and 18 (HPV16/18) and performed RT-qPCR. We found that Nanog increases activity of both viral regulatory regions and elevates endogenous E6/E7 mRNA levels in cervical cancer-de
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Amador-Molina, Alfredo, José Luis González-Montoya, Alejandro García-Carrancá, Alejandro Mohar, and Marcela Lizano. "Intratypic changes of the E1 gene and the long control region affect ori function of human papillomavirus type 18 variants." Journal of General Virology 94, no. 2 (February 1, 2013): 393–402. http://dx.doi.org/10.1099/vir.0.045807-0.

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A persistent infection with high-risk human papillomavirus (HPV) constitutes the main aetiological factor for cervical cancer development. HPV16 and 18 are the most prevalent types found in cervical cancer worldwide. It has been proposed that HPV intratype variations may result in differences in biological behaviour. Three different HPV18 variants belonging to the Asian Amerindian (AsAi), European (E) and African (Af) branches have been associated with specific histological types of cervical cancer with different relative prognoses, suggesting that HPV18 genomic variations might participate in
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Lina Villa, Luisa, and Richard Schlegel. "Differences in transformation activity between HPV-18 and HPV-16 map to the viral LCR-E6-E7 region." Virology 181, no. 1 (March 1991): 374–77. http://dx.doi.org/10.1016/0042-6822(91)90507-8.

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Martínez, Rocio Susana Méndez, Norma Rivera-Martínez, Juan G. Sierra-Madero, David Cantú de León, and Alejandro García-Carranca. "23. Prevalence of virus infection of human papillomavirus and identification of variants in the anal canal of men who have sex with men HIV-positive in Mexico." Sexual Health 10, no. 6 (2013): 581. http://dx.doi.org/10.1071/shv10n6ab23.

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Background Men who have sex with men (MSM) have been identified as a high-risk group for anal cancer. HPV has been found associated with this neoplasia as it has been in cervical cancer. Concurrent infection with HIV may facilitate or accelerate the pathological consequences of HPV infections. In Mexico, where cervical cancer is a major public health problem, little is known about the prevalence of anal cancer and the role of HPV in the HIV-positive population of MSM. Methods: We analysed 323 anal exudates from HIV-positive MSM, from the HIV Clinic at Instituto Nacional de Ciencias Médicas y N
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Munsamy, Yuri, Riaz Y. Seedat, Tumelo R. Sekee, Phillip A. Bester, and Felicity J. Burt. "Complete genome sequence of a HPV31 isolate from laryngeal squamous cell carcinoma and biological consequences for p97 promoter activity." PLOS ONE 16, no. 8 (August 25, 2021): e0252524. http://dx.doi.org/10.1371/journal.pone.0252524.

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Human papillomavirus type 31, although detected less frequently than HPV types 16 and 18, is associated with head and neck squamous cell carcinomas. Previous studies suggest that polymorphisms in the long control region (LCR) may alter the oncogenic potential of the virus. This study reports the first complete genome of a South African HPV31 isolate from a laryngeal squamous cell carcinoma. Sequence variations relative to the HPV31 prototype sequence were identified. The pBlue-Topo® vector, a reporter gene system was used to investigate the possible influence of these variations on the LCR pro
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Tan, Shyh-Han, Dusan Bartsch, Elisabeth Schwarz, and Hans-Ulrich Bernard. "Nuclear Matrix Attachment Regions of Human Papillomavirus Type 16 Point toward Conservation of These Genomic Elements in All Genital Papillomaviruses." Journal of Virology 72, no. 5 (May 1, 1998): 3610–22. http://dx.doi.org/10.1128/jvi.72.5.3610-3622.1998.

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ABSTRACT The gene functions, transcriptional regulation, and genome replication of human papillomaviruses (HPVs) have been extensively studied. Thus far, however, there has been little research on the organization of HPV genomes in the nuclei of infected cells. As a first step to understand how chromatin and suprachromatin structures may modulate the life cycles of these viruses, we have identified and mapped interactions of HPV DNAs with the nuclear matrix. The endogenous genomes of HPV type 16 (HPV-16) which are present in SiHa, HPKI, and HPKII cells, adhere in vivo to the nuclear matrixes o
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Chen, Alyce A., Tarik Gheit, Silvia Franceschi, Massimo Tommasino, and Gary M. Clifford. "Human Papillomavirus 18 Genetic Variation and Cervical Cancer Risk Worldwide." Journal of Virology 89, no. 20 (August 12, 2015): 10680–87. http://dx.doi.org/10.1128/jvi.01747-15.

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ABSTRACTHuman papillomavirus 18 (HPV18) is the second most carcinogenic HPV type, after HPV16, and it accounts for approximately 12% of squamous cell carcinoma (SCC) as well as 37% of adenocarcinoma (ADC) of the cervix worldwide. We aimed to evaluate the worldwide diversity and carcinogenicity of HPV18 genetic variants by sequencing the entire long control region (LCR) and the E6 open reading frame of 711 HPV18-positive cervical samples from 39 countries, taking advantage of the International Agency for Research on Cancer biobank. A total of 209 unique HPV18 sequence variants were identified t
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Turner, S., C. Studwell, S. Deharvengt, K. D. Lyons, J. A. Plata, E. LaRochelle, A. M. Zapata, L. Kennedy, and S. Bejarano. "High-Risk HPV Genotypes Identified in Northern Honduras: Evidence for Prevention." Journal of Global Oncology 4, Supplement 2 (October 1, 2018): 211s. http://dx.doi.org/10.1200/jgo.18.85200.

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Background: Cervical cancer is one of the most prevalent cancers in Honduran women. Lacking national or population-based registries, we rely on hospital registries to establish incidence: San Felipe General Hospital in 2012 diagnosed 38% of 998 women and The League against Cancer Hospital (LCC) in 2016 diagnosed 54.4% of 695 women with cervical cancer CC. According to PAHO's Honduras Profile 2013, screening coverage with Pap was 48.1%. Bruni in 2010 reported a prevalence of high risk HPV (hrHPV) infection for Central America of 13%, identifying genotypes 16, 18, 52, 31 and 58 as most frequent.
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Rozprawy doktorskie na temat "HPV-18 LCR"

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Lung, Mandy Siu Yu Biotechnology &amp Biomolecular Sciences Faculty of Science UNSW. "The use of Human Papillomavirus promoters to target Cervical Cancer cells." Publisher:University of New South Wales. Biotechnology & Biomolecular Sciences, 2008. http://handle.unsw.edu.au/1959.4/42610.

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Human Papillomavirus (HPV) is one of the most common causes of sexually transmitted disease worldwide. Infections by high-risk HPVs, such as HPV-18, have been associated etiologically with cervical cancer. The successful development of HPV vaccines may be beneficial to the HPV-na??ve population, but women that have already been exposed to the virus are still at risk of developing HPV-associated malignancies. A need for a systemic cure for HPV-infection therefore still exists. Gene therapies using tissue-specific promoters have been reported to be a promising tool for treating cancers; however,
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