Academic literature on the topic 'Reverse-trancription'

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Journal articles on the topic "Reverse-trancription"

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Wiggins, Kathryn J., Renae M. Gow, John Kanellis, Prue Hill, Darren J. Kelly, Alison Skene, David J. Goodman, and Robyn G. Langham. "BK virus RNA can be detected in archival renal transplant biopsies using the reverse trancription polymerase chain reaction." Nephrology Dialysis Transplantation 24, no. 2 (December 4, 2008): 661–66. http://dx.doi.org/10.1093/ndt/gfn656.

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Pal, Utpal, Penghua Wang, Fukai Bao, Xiuli Yang, Swapna Samanta, Robert Schoen, Gary P. Wormser, Ira Schwartz, and Erol Fikrig. "Borrelia burgdorferi basic membrane proteins A and B participate in the genesis of Lyme arthritis." Journal of Experimental Medicine 205, no. 1 (December 31, 2007): 133–41. http://dx.doi.org/10.1084/jem.20070962.

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Lyme arthritis results from colonization of joints by Borrelia burgdorferi and the ensuing host response. Using gene array–based differential analysis of B. burgdorferi gene expression and quantitative reverse trancription-polymerase chain reaction, we identified two paralogous spirochete genes, bmpA and bmpB, that are preferentially up-regulated in mouse joints compared with other organs. Transfer of affinity-purified antibodies against either BmpA or BmpB into B. burgdorferi–infected mice selectively reduced spirochete numbers and inflammation in the joints. B. burgdorferi lacking bmpA/B were therefore generated to further explore the role of these proteins in the pathogenesis of Lyme disease. B. burgdorferi lacking bmpA/B were infectious in mice, but unable to persist in the joints, and they failed to induce severe arthritis. Complementation of the mutant spirochetes with a wild-type copy of the bmpA and bmpB genes partially restored the original phenotype. These data delineate a role for differentially produced B. burgdorferi antigens in spirochete colonization of mouse joints, and suggest new strategies for the treatment of Lyme arthritis.
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Liu, Sihai, Jing Zhang, Ting Zheng, Xiongneng Mou, and Wenwei Xin. "Circ_WWC3 overexpression decelerates the progression of osteosarcoma by regulating miR-421/PDE7B axis." Open Life Sciences 16, no. 1 (January 1, 2021): 229–41. http://dx.doi.org/10.1515/biol-2021-0021.

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Abstract Background Emerging evidence has shown that circular RNAs (circRNAs) are vital regulators in osteosarcoma (OS) progression. However, the effects of circ_WWC3 in OS have not been explored. In this research, the functions and mechanisms of circ_WWC3 in OS were investigated. Methods Quantitative reverse trancription polymerase chain reaction (qRT-PCR) was adopted to determine the levels of circ_WWC3, WW and WWC3 mRNA, miR-421, and phosphodiesterase 7B (PDE7B) mRNA. RNase R assay was used to determine the characteristic of circ_WWC3. Colony formation assay and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay were applied for cell growth. Transwell assay was performed for cell migration and invasion. Flow cytometry analysis was utilized for cell apoptosis. Western blot assay was conducted for the levels of apoptosis-related proteins and PDE7B protein. Dual-luciferase reporter assay was carried out to analyze the targeting relationship between miR-421 and circ_WWC3 or PDE7B. The murine xenograft model was established to explore the effect of circ_WWC3 in vivo. Results Compared to normal tissues and cells, circ_WWC3 and PDE7B were downregulated in OS tissues and cells. Overexpression of circ_WWC3 or PDE7B suppressed OS cell growth, migration, and invasion and promoted apoptosis in vitro. Regarding the mechanism analysis, circ_WWC3 positively modulated PDE7B expression by targeting miR-421. MiR-421 overexpression restored the impacts of circ_WWC3 on OS cell growth, metastasis, and apoptosis. Inhibition of miR-421 repressed the malignant behaviors of OS cells by targeting PDE7B. In addition, circ_WWC3 inhibited the tumorigenicity of OS in vivo. Conclusion Circ_WWC3 overexpression slowed the development of OS by elevating PDE7B via sponging miR-421.
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Budiarti, Retno, Siti Qamariyah Khairunisa, Nasronudin, Kuntaman, and Guritno. "Hyperbaric hyperoxia exposure in suppressing human immunodeficiencyvirus replication: An experimental in vitro in peripheral mononuclear blood cells culture." Infectious Disease Reports, July 7, 2020. http://dx.doi.org/10.4081/idr.2020.8743.

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Cellular immune has an important role in response HIV infection, which is attack the infected cells to activate signaling molecule. Hyperbaric Oxygen (HBO) worked as complementary treatment for HIV infection. The production of ROS and RNS molecules during hyperbaric exposure can affect gene expression which contributes to cellular adaptative response. This study was conducted to explore the mechanisms of cellular adaptive response to HIV infection during hyperbaric exposure. This study was carried on in vitro using healthy volunteers’ PBMCs (Peripheral Blood Mononuclear Cells) cultures infected with HIV-1. The study was conducted as a post- test only group design. The experimental unit was PBMC from venous blood of healthy volunteers which were cultured in vitro and infected by co-culturing with HIV-1 in MT4 cell line. The experimental unit consist of treatment and control group. Each group examined the expression of transcription factor NFκB, Interferon α, reverse transcriptase inhibitors (p21), and the amount of HIV-1 p24 antigen. There were increasingly significant differences in the expression of the trancription factor of NFκB, p21, and HIV-1 p24 antigen,as well as mRNA transcription of interferon α2 between treatment and controlgroup. By decreasing p24 antigen showed that HBO exposure was able to suppress HIV-1 replication. The exposure to hyperbaric oxygen at the pressure of 2.4 ATAand 98% oxygen wasable to produce ROS and RNS molecules, which play a role in cellular adaptive responses through increasing the expression of nfĸb, p21 and mRNA of interferon α2 plays a role in inhibition mechanism of HIV-1 replication in cells.
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Dissertations / Theses on the topic "Reverse-trancription"

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Villalva, Grégoire Claire. "Profil d'expression génique dans les lymphomes anaplasiques à grandes cellules NPM-ALK positifs." Toulouse 3, 2004. http://www.theses.fr/2004TOU30201.

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Dans les lymphomes anaplasiques à grandes cellules, la translocation t(2;5)(p23;q35) conduit à l'expression aberrante de la protéine NPM-ALK (Nucléophosmine-Anaplastic Lymphoma Kinase). Nous avons voulu étudier les gènes dérégulés dans ces lymphomes par la technique de SSH (Subtractive Suppressive Hybridization). La première étape est la reverse-transcription des ARNm. Nous avons montré que le rendement de cette étape pouvait être augmenté en ajoutant la protéine T4 gene 32. La SSH a été effectuée à partir d'une lignée de lymphome anaplasique portant la translocation comparée à des cellules d'un patient porteur de la tumeur sans translocation. Nous avons obtenu 92 clones et le séquençage nous a permis d'identifier 31 gènes sur-exprimés dans la lignée t(2;5) positive. Le profil d'expression se caractérise par des gènes de survie cellulaire. Certains sont impliqués dans la signalisation médiée par la PI-3 kinase décrite comme effectrice de la voie médiée par NPM-ALK.
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