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Relevant bibliographies by topics / Moloney murine leukemia virus; Therapy / Dissertations / Theses

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Dissertations / Theses on the topic 'Moloney murine leukemia virus; Therapy'

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Published: 4 June 2021

Last updated: 15 February 2022

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1

Ismail, Said. "Development of novel MoMLV gene transfer systems by exploiting retroviral RNA processing." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365806.

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2

Vasser, Geneva M. "Manipulation of the moloney murine leukemia virus envelope protein in an effort to develop directly and indirectly targeted retroviral vectors for use in human gene therapy." View the abstract Download the full-text PDF version, 2008. http://etd.utmem.edu/ABSTRACTS/2008-031-Vasser-Index.html.

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Thesis (M.S. )--University of Tennessee Health Science Center, 2008
Title from title page screen (viewed on Sept. 17, 2008). Research advisor: Lorraine M. Albritton, Ph.D. Document formatted into pages (x, 138 p. : ill.). Vita. Abstract. Includes bibliographical references (p. 40-48).

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3

Wallin, Michael. "Fusion activation in murine leukemia virus /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-748-0/.

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4

Koepke, Kristine Ann. "Expression and characterization of integrase from Moloney murine leukemia virus." Thesis, University of Bath, 1994. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359638.

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5

Klimowicz, Alexander Charles. "Pseudotyping the Moloney murine leukemia virus with engineered envelope glycoproteins." Thesis, University of Ottawa (Canada), 2001. http://hdl.handle.net/10393/9297.

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We were interested in generating an in vivo retroviral gene therapy vector based on the commonly used Moloney murine leukemia virus (MoMLV). This was accomplished by pseudotyping with an engineered influenza A hemagglutinin. Point mutations were introduced to abrogate hemagglutinin's wild type binding and a single chain variable domain antibody fragment (scFv) was added to its amino terminus to provide new binding specificity. The engineered hemagglutinin was able to mediate binding of pseudotyped retrovirus to a scFv specific peptide but was unable mediate infection of target cells. To rescue the infectivity of the pseudotyped retrovirus the role of lipid rafts in the lifecycle of the MoMLV was examined. Lipid raft isolation from transfected cells and virus particles revealed that retroviral proteins were not associated with lipid rafts. Using a panel of hemagglutinin mutants with reduced lipid raft affinity we also determined that this parameter did not affect pseudotyping efficiency.

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6

Hamirally, Sofia. "Mechanistic studies of the translational readthrough signal of Moloney murine leukemia virus." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619933.

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7

Villeneuve, Luc. "Insertional mutagenesis by provirus integration in Moloney murine leukemia virus-induced rat thymomas." Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=74060.

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8

Konishi, Atsushi. "Studies on the thermostabilization of reverse transcriptases from Moloney murine leukemia virus and avian myeloblastosis virus." Kyoto University, 2015. http://hdl.handle.net/2433/199340.

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Kyoto University (京都大学)
0048
新制・課程博士
博士(農学)
甲第19016号
農博第2094号
新制||農||1029(附属図書館)
学位論文||H27||N4898(農学部図書室)
31967
京都大学大学院農学研究科食品生物科学専攻
(主査)教授保川清, 教授河田照雄, 教授谷史人
学位規則第4条第1項該当

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9

Bae, Youngmee. "Study on the surface protein of Moloney murine leukaemia virus (Mo-MuLV), GP70." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320614.

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10

Zedeler, Anne. "Palmitoylation and raft localization of the retrovirus Moloney MLV R-peptide studied by mutagenesis : PhD thesis /." Cph. : Department of Pharmacology, The Danish University of Pharmaceutical Sciences, 2005. http://www.dfuni.dk/index.php/Anne_Zedeler/1733/0/.

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11

Bagalb, Hussein Saeed. "Cellular and molecular biological studies of a retroviral induced lymphoma transmitted via breast milk in a mouse model." Connect to full text in OhioLINK ETD Center, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1225294363.

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Thesis (M.S.)--University of Toledo, 2008.
"In partial fulfillment of the requirements for the degree of Master of Science in Biomedical Sciences." Title from title page of PDF document. Bibliography: pages 82-88, 111-116.

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12

Johansson, Ann-Sofie. "Establishment and characterization of a murine T-cell lymphoma/leukemia model." Doctoral thesis, Umeå universitet, Institutionen för strålningsvetenskaper, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-35195.

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Mouse models of human disease are valuable tools for studying pathogenesis and for evaluating novel therapies. T-cell lymphoma is a relatively rare disease in humans, affecting 100-150 persons yearly in Sweden. It exists in both aggressive and more indolent forms. We have established a mouse model for an aggressive T-cell lymphoma, the T-cell lymphoma/leukemia (TLL) mouse. In the present thesis, the TLL mouse model was characterized and used for experimental therapeutic and primary prevention studies. The TLL mouse was established unintentionally in our laboratory during work on VH-gene replacement in a “knock-in” mouse experimental setting. The generated chimeras all developed aggressive T-cell lymphomas affecting the lymphoid organs, lungs, kidneys and liver. The lymphoma phenotype segregated from the targeted locus and we could demonstrate the presence of Moloney murine leukemia virus (MMLV) in the germline of the affected mice. MMLV is a retrovirus known to induce T-cell lymphomas when inoculated in newborn mice. We further characterized two TLL substrains; TLL-2 and TLL-14 carrying the proviral integrations on chromosomes 2 and 14 respectively. Significant differences were found between the substrains regarding lymphoma frequency and immunophenotype, the TLL-14 substrain developing tumors with higher frequency than TLL-2 and with a more mature immunophenotype. A transfer model was developed in which TLL cells could be readily transferred intravenously to syngenic recipients causing aggressive lymphomas. The transfer model was used in a therapeutic study where the selective COX-2 inhibitor celecoxib was evaluated as a single agent and in combination with the established anti-tumor agent cyclophosphamide. The study was based on results from other tumor types that have indicated celecoxib, originally an anti-inflammatory and analgetic drug, to have possible anti-tumor effects. In our TLL model, however, we could not demonstrate any benefit of celecoxib monotherapy or any additive effect to cyclophosphamide. Dietary fatty acids, in particular omega-3 fatty acids, have been a focus of public and scientific interest due to observed effects on the prevention of cardiovascular disease, cancer and inflammatory conditions. In addition, omega-3 fatty acids inhibit T-cell proliferation in vitro. We supplemented the diet of TLL mice with omega-3 and omega-6 fatty acids respectively and could demonstrate a significant delay in lymphoma onset between 5-8 months of age in the group receiving an omega-3 rich diet.

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13

Hammarstedt, Maria. "Incorporation of cellular proteins into enveloped virus particles /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-966-1/.

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14

Whiting, Sam H. "Studies into the characteristics and mechanism of strand displacement synthesis by retroviral reverse transcriptase /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/11494.

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15

Kelleher, Colleen Diane. "Characterization of polymerase and RNase H activities of Moloney murine leukemia virus reverse transcriptase in relation to models for retroviral plus-strand synthesis /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/11519.

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16

Delviks, Krista Anda. "Development of murine leukemia virus-based vectors for more effective gene therapy genetic analysis of direct repeat deletions /." Morgantown, W. Va. : [West Virginia University Libraries], 1999. http://etd.wvu.edu/templates/showETD.cfm?recnum=642.

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Thesis (Ph. D.)--West Virginia University, 1999.
Title from document title page. Document formatted into pages; contains vi, 119 p. : ill. Vita. Includes abstract. Includes bibliographical references.

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17

Silveira, Giórgia Gobbi da. "Relação entre o gene B-Cell-Specific Moloney Murine Leukemia Virus Integration Site 1 (BMI-1) e genes reguladores da recombinação homóloga em carcinomas ductais invasores da mama." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/17/17143/tde-08082014-112232/.

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Bmi-1 é uma proteína do grupo Polycomb capaz de induzir atividade de telomerase, levando à imortalização de células epiteliais. As células, quando imortalizadas, se tronam mais susceptíveis a danos em dupla fita (double-strand breaks (DSB))e a recombinação homóloga é uma das duas vias de reparo dos DSBs. Dentre os genes reguladores da recombinação homóloga temos o BRCA-1, que está envolvido na resposta ao dano associado à proteína RAD51, que por sua vez se acumula rapidamente nos focos de dano ao DNA após a sinalização do H2AX, que têm se mostrado um excelente marcador de dano celular por se acumular rapidamente nos focos de lesão, desencadeando o processo de reparo. Topoisomerase III (TopoIII) remove intermediários da recombinação homóloga antes da segregação de cromossomos, prevenindo danos à estrutura do DNA celular. O papel das proteínas envolvidas na recombinação homóloga, em carcinomas ductais invasores positivos para o BMI-1, necessita ser investigado. Utilizando-se tissue microarrays contendo 239 casos de carcinomas ductais mamários primários, foi analisada a expressão imunoistoquímica de BMI-1, receptor de estrógeno, receptor de progesterona, HER-2, Ki67, p53 e BRCA-1, H2AX, RAD51 e topoisomerase III. Positividade para o Bmi-1 foi encontrada em 66 casos (27.6%). A positividade imunoistoquímica do BMI-1 relacionou-se a RE (p=0,004), RP (p<0,001), Ki-67 (p < 0,001), p53 (p=0,003), BRCA-1(p= 0,003), H2AX (p= 0,024) e TopoIII (p < 0,001). Concluindo, nossos resultados mostraram haver relação entre o BMI-1 e genes reguladores da HR, sugerindo que a positividade de BMI-1 pode ser um importante evento na recombinação homóloga em carcinomas ductais invasores da mama.
Bmi-1 is a Polycomb group protein which is able to induce telomerase activity, enabling the immortalization of epithelial cells. Immortalized cells shown more susceptible to double-strand breaks (DSB) and the homologous recombination (HR) are one of DSB repair pathways. Among the regulatory genes in HR, there is BRCA1, involved in the response to DNA damage associated with the RAD51 protein, which accumulates in DNA damage foci after signaling H2AX. H2AX has also been shown to be a good marker of DNA damage. Topoisomerase III (TopoIII) removes HR intermediates before the segregation of chromosomes, preventing damage to the structure of the cellular DNA. The role of proteins involved in HR, in breast carcinomas positive for BMI-1, remains to be investigated. The aim of this study was evaluate the association between BMI-1 and homologous recombination proteins. Using tissue microarrays containing 239 cases of primary breast tumors, the expression of Bmi-1, BRCA-1, H2AX, Rad51, p53, Ki-67, topoisomerase III, RE, RP and HER-2 was analyzed by immunohistochemistry. We observe high expression of Bmi-1 in 66 cases (27.6%). Immunohistochemistry overexpression of BMI-1 was related to RE (p=0,004), RP (p<0,001), Ki-67 (p < 0,001), p53 (p=0,003), BRCA-1(p= 0,003), H2AX (p= 0,024) and TopoIII (p < 0,001). Our results showed a relation between the expression of BMI-1 and HR regulatory genes, suggesting that overexpression of Bmi-1 is an important event in breast cancer homologous recombination.

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18

Rosales, Gerpe María Carla. "The Role of APOBEC3 in Controlling Retroviral Spread and Zoonoses." Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31484.

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APOBEC3 (A3) proteins are a family of host-encoded cytidine deaminases that protect against retroviruses and other viral intruders. Retroviruses, unlike other viruses, are able to integrate their genomic proviral DNA within hours of entering host cells. A3 proteins hinder retroviral infectivity by editing retroviral replication intermediates, as well as by inhibiting retroviral replication and integration through deamination-independent methods. These proteins thus constitute the first line of immune defense against endogenous and exogenous retroviral pathogens. The overall goal of my Master's project was to better understand the critical role A3 proteins play in restricting inter- and intra-host transmission of retroviruses. There are two specific aspects that I focused on: first, investigating the role of mouse APOBEC3 (mA3) in limiting the zoonotic transmission of murine leukemia retroviruses (MLVs) in a rural environment; second, to identify the molecular features in MLVs that confer susceptibility or resistance to deamination by mA3. For the first part of my project, we collected blood samples from dairy and production cattle from four different geographical locations across Canada. We then designed a novel PCR screening strategy targeting conserved genetic regions in MLVs and Mouse Mammary Tumor Virus (MMTV) and MMTV-like betaretroviruses. Our results indicate that 4% of animals were positive for MLV and 2% were positive for MMTV. Despite crossing the species barrier by gaining entry into bovine cells, our study also demonstrates that the bovine A3 protein is able to potently inhibit the spread of these murine retroviruses in vitro. The next question we asked was whether mA3 could also mutate and restrict murine endogenous retroviruses and thereby partake in limiting zoonotic transmission. Moloney MLV and AKV MLV are two highly homologous murine gammaretroviruses with opposite sensitivities to restriction by mA3: MoMLV is resistant to restriction and deamination while AKV is sensitive to both. Design of MoMLV/AKV hybrid viruses enabled us to map the region of mA3 resistance to the region encoding the glyco-Gag accessory protein. Site-directed mutagenesis then allowed us to correlate the number of N-linked glycosylation sites with the level of resistance to deamination by mA3. Our results suggest that Gag glycosylation is a possible viral defence mechanism that arose to counteract the evolutionary pressure imposed by mA3. Overall, my projects show the important role A3 proteins play in intrinsic immunity, whether defending the host from foreign retroviral invaders or endogenous retroviral foes.

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19

Pan, Jiun Tyng, and 潘俊廷. "Mutation and deletion on Moloney murine leukemia virus." Thesis, 1995. http://ndltd.ncl.edu.tw/handle/17329604966598680030.

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20

Peng, Wen-Jiun, and 彭文君. "Target integration by a chimeric Sp1 zinc finger domain/Moloney murine leukemia virus integrase protein in vivo." Thesis, 2000. http://ndltd.ncl.edu.tw/handle/96391337074990832044.

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21

Vu, Halong Nguyen. "Engineering viruses for gene therapy : isolating and characterizing murine leukemia virus with improved stability /." 2006. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3223740.

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Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2006.
Source: Dissertation Abstracts International, Volume: 67-07, Section: B, page: 3961. Adviser: Daniel W. Pack. Includes bibliographical references. Available on microfilm from Pro Quest Information and Learning.

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22

Lai, Ming Chih, and 賴銘志. "Cloning of HIV-1 Integrase into a Moloney Murine Leukemia Virus Based Vector to Establish a Cell Line for In Vivo Integration Assay of HIV-1 Integrase." Thesis, 1994. http://ndltd.ncl.edu.tw/handle/48848916245915300130.

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