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Опубліковано: 6 вересня 2023

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Статті в журналах з теми "RETROVIRAL PROTEASE"

1

Blusch, Jürgen H., Sigrid Seelmeir, and Klaus von der Helm. "Molecular and Enzymatic Characterization of the Porcine Endogenous Retrovirus Protease." Journal of Virology 76, no. 15 (August 1, 2002): 7913–17. http://dx.doi.org/10.1128/jvi.76.15.7913-7917.2002.

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ABSTRACT The protease of the porcine endogenous retrovirus (PERV) subtypes A/B and C was recombinantly expressed in Escherichia coli as proteolytically active enzyme and characterized. The PERV Gag precursor was also recombinantly produced and used as the substrate in an in vitro enzyme assay in parallel with synthetic nonapeptide substrates designed according to cleavage site sequences identified in the PERV Gag precursor. The proteases of all PERV subtypes consist of 127 amino acid residues with an M r of 14,000 as revealed by determining the protease N and C termini. The PERV proteases have a high specificity for PERV substrates and do not cleave human immunodeficiency virus (HIV)-specific substrates, nor are they inhibited by specific HIV protease inhibitors. Among the known retroviral proteases, the PERV proteases resemble most closely the protease of the murine leukemia retrovirus.
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2

Lehmann-Che, Jacqueline, Marie-Lou Giron, Olivier Delelis, Martin Löchelt, Patricia Bittoun, Joelle Tobaly-Tapiero, Hugues de Thé, and Ali Saïb. "Protease-Dependent Uncoating of a Complex Retrovirus." Journal of Virology 79, no. 14 (July 2005): 9244–53. http://dx.doi.org/10.1128/jvi.79.14.9244-9253.2005.

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ABSTRACT Although retrovirus egress and budding have been partly unraveled, little is known about early stages of the replication cycle. In particular, retroviral uncoating, a process during which incoming retroviral cores are altered to allow the integration of the viral genome into host chromosomes, is poorly understood. To get insights into these early events of the retroviral cycle, we have used foamy complex retroviruses as a model. In this report, we show that a protease-defective foamy retrovirus is noninfectious, although it is still able to bud and enter target cells efficiently. Similarly, a retrovirus mutated in an essential viral protease-dependent cleavage site in the central part of Gag is noninfectious. Following entry, wild-type and mutant retroviruses are able to traffic along microtubules towards the microtubule-organizing center (MTOC). However, whereas nuclear import of Gag and of the viral genome was observed for the wild-type virus as early as 8 hours postinfection, incoming capsids and genome from mutant viruses remained at the MTOC. Interestingly, a specific viral protease-dependent Gag cleavage product was detected only for the wild-type retrovirus early after infection, demonstrating that cleavage of Gag by the viral protease at this stage of the virus life cycle is absolutely required for productive infection, an unprecedented observation among retroviruses.
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3

Davis, David A., Cara A. Brown, Fonda M. Newcomb, Emily S. Boja, Henry M. Fales, Joshua Kaufman, Stephen J. Stahl, Paul Wingfield, and Robert Yarchoan. "Reversible Oxidative Modification as a Mechanism for Regulating Retroviral Protease Dimerization and Activation." Journal of Virology 77, no. 5 (March 1, 2003): 3319–25. http://dx.doi.org/10.1128/jvi.77.5.3319-3325.2003.

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ABSTRACT Human immunodeficiency virus protease activity can be regulated by reversible oxidation of a sulfur-containing amino acid at the dimer interface. We show here that oxidation of this amino acid in human immunodeficiency virus type 1 protease prevents dimer formation. Moreover, we show that human T-cell leukemia virus type 1 protease can be similarly regulated through reversible glutathionylation of its two conserved cysteine residues. Based on the known three-dimensional structures and multiple sequence alignments of retroviral proteases, it is predicted that the majority of retroviral proteases have sulfur-containing amino acids at the dimer interface. The regulation of protease activity by the modification of a sulfur-containing amino acid at the dimer interface may be a conserved mechanism among the majority of retroviruses.
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4

Weber, Irene T., Yuan-Fang Wang, and Robert W. Harrison. "HIV Protease: Historical Perspective and Current Research." Viruses 13, no. 5 (May 6, 2021): 839. http://dx.doi.org/10.3390/v13050839.

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The retroviral protease of human immunodeficiency virus (HIV) is an excellent target for antiviral inhibitors for treating HIV/AIDS. Despite the efficacy of therapy, current efforts to control the disease are undermined by the growing threat posed by drug resistance. This review covers the historical background of studies on the structure and function of HIV protease, the subsequent development of antiviral inhibitors, and recent studies on drug-resistant protease variants. We highlight the important contributions of Dr. Stephen Oroszlan to fundamental knowledge about the function of the HIV protease and other retroviral proteases. These studies, along with those of his colleagues, laid the foundations for the design of clinical inhibitors of HIV protease. The drug-resistant protease variants also provide an excellent model for investigating the molecular mechanisms and evolution of resistance.
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5

Pettit, Steven C., Sergei Gulnik, Lori Everitt, and Andrew H. Kaplan. "The Dimer Interfaces of Protease and Extra-Protease Domains Influence the Activation of Protease and the Specificity of GagPol Cleavage." Journal of Virology 77, no. 1 (January 1, 2003): 366–74. http://dx.doi.org/10.1128/jvi.77.1.366-374.2003.

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ABSTRACT Activation of the human immunodeficiency virus type 1 (HIV-1) protease is an essential step in viral replication. As is the case for all retroviral proteases, enzyme activation requires the formation of protease homodimers. However, little is known about the mechanisms by which retroviral proteases become active within their precursors. Using an in vitro expression system, we have examined the determinants of activation efficiency and the order of cleavage site processing for the protease of HIV-1 within the full-length GagPol precursor. Following activation, initial cleavage occurs between the viral p2 and nucleocapsid proteins. This is followed by cleavage of a novel site located in the transframe domain. Mutational analysis of the dimer interface of the protease produced differential effects on activation and specificity. A subset of mutations produced enhanced cleavage at the amino terminus of the protease, suggesting that, in the wild-type precursor, cleavages that liberate the protease are a relatively late event. Replacement of the proline residue at position 1 of the protease dimer interface resulted in altered cleavage of distal sites and suggests that this residue functions as a cis-directed specificity determinant. In summary, our studies indicate that interactions within the protease dimer interface help determine the order of precursor cleavage and contribute to the formation of extended-protease intermediates. Assembly domains within GagPol outside the protease domain also influence enzyme activation.
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6

Youngren, S. D., J. D. Boeke, N. J. Sanders, and D. J. Garfinkel. "Functional organization of the retrotransposon Ty from Saccharomyces cerevisiae: Ty protease is required for transposition." Molecular and Cellular Biology 8, no. 4 (April 1988): 1421–31. http://dx.doi.org/10.1128/mcb.8.4.1421-1431.1988.

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We used several mutations generated in vitro to further characterize the functions of the products encoded by the TyB gene of the transpositionally active retrotransposon TyH3 from Saccharomyces cerevisiae. Mutations close to a core protein domain of TyB, which is homologous to retroviral proteases, have striking effects on Ty protein processing, the physiology of Ty viruslike particles, and transposition. The Ty protease is required for processing of both TyA and TyB proteins. Mutations in the protease resulted in the synthesis of morphologically and functionally aberrant Ty viruslike particles. The mutant particles displayed reverse transcriptase activity, but did not synthesize Ty DNA in vitro. Ty RNA was present in the mutant particles, but at very low levels. Transposition of a genetically tagged element ceased when the protease domain was mutated, demonstrating that Ty protease is essential for transposition. One of these mutations also defined a segment of TyB encoding an active reverse transcriptase. These results indicate that the Ty protease, like its retroviral counterpart, plays an important role in particle assembly, replication, and transposition of these elements.
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7

Youngren, S. D., J. D. Boeke, N. J. Sanders, and D. J. Garfinkel. "Functional organization of the retrotransposon Ty from Saccharomyces cerevisiae: Ty protease is required for transposition." Molecular and Cellular Biology 8, no. 4 (April 1988): 1421–31. http://dx.doi.org/10.1128/mcb.8.4.1421.

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Анотація:
We used several mutations generated in vitro to further characterize the functions of the products encoded by the TyB gene of the transpositionally active retrotransposon TyH3 from Saccharomyces cerevisiae. Mutations close to a core protein domain of TyB, which is homologous to retroviral proteases, have striking effects on Ty protein processing, the physiology of Ty viruslike particles, and transposition. The Ty protease is required for processing of both TyA and TyB proteins. Mutations in the protease resulted in the synthesis of morphologically and functionally aberrant Ty viruslike particles. The mutant particles displayed reverse transcriptase activity, but did not synthesize Ty DNA in vitro. Ty RNA was present in the mutant particles, but at very low levels. Transposition of a genetically tagged element ceased when the protease domain was mutated, demonstrating that Ty protease is essential for transposition. One of these mutations also defined a segment of TyB encoding an active reverse transcriptase. These results indicate that the Ty protease, like its retroviral counterpart, plays an important role in particle assembly, replication, and transposition of these elements.
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8

Álvarez, Enrique, Luis Menéndez-Arias, and Luis Carrasco. "The Eukaryotic Translation Initiation Factor 4GI Is Cleaved by Different Retroviral Proteases." Journal of Virology 77, no. 23 (December 1, 2003): 12392–400. http://dx.doi.org/10.1128/jvi.77.23.12392-12400.2003.

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ABSTRACT The initiation factor eIF4G plays a central role in the regulation of translation. In picornaviruses, as well as in human immunodeficiency virus type 1 (HIV-1), cleavage of eIF4G by the viral protease leads to inhibition of protein synthesis directed by capped cellular mRNAs. In the present work, cleavage of both eIF4GI and eIF4GII has been analyzed by employing the proteases encoded within the genomes of several members of the family Retroviridae, e.g., Moloney murine leukemia virus (MoMLV), mouse mammary tumor virus, human T-cell leukemia virus type 1, HIV-2, and simian immunodeficiency virus. All of the retroviral proteases examined were able to cleave the initiation factor eIF4GI both in intact cells and in cell-free systems, albeit with different efficiencies. The eIF4GI hydrolysis patterns obtained with HIV-1 and HIV-2 proteases were very similar to each other but rather different from those obtained with MoMLV protease. Both eIF4GI and eIF4GII were cleaved very efficiently by the MoMLV protease. However, eIF4GII was a poor substrate for HIV proteases. Proteolytic cleavage of eIF4G led to a profound inhibition of cap-dependent translation, while protein synthesis driven by mRNAs containing internal ribosome entry site elements remained unaffected or was even stimulated in transfected cells.
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9

Hartl, Maximilian J., Kristian Schweimer, Martin H. Reger, Stephan Schwarzinger, Jochen Bodem, Paul Rösch, and Birgitta M. Wöhrl. "Formation of transient dimers by a retroviral protease." Biochemical Journal 427, no. 2 (March 29, 2010): 197–203. http://dx.doi.org/10.1042/bj20091451.

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Retroviral proteases have been shown previously to be only active as homodimers. They are essential to form the separate and active proteins from the viral precursors. Spumaretroviruses produce separate precursors for Gag and Pol, rather than a Gag and a Gag–Pol precursor. Nevertheless, processing of Pol into a PR (protease)–RT (reverse transcriptase) and integrase is essential in order to obtain infectious viral particles. We showed recently that the PR–RT from a simian foamy virus, as well as the separate PRshort (protease) domain, exhibit proteolytic activities, although only monomeric forms could be detected. In the present study, we demonstrate that PRshort and PR–RT can be inhibited by the putative dimerization inhibitor cholic acid. Various other inhibitors, including darunavir and tipranavir, known to prevent HIV-1 PR dimerization in cells, had no effect on foamy virus protease in vitro. 1H-15N HSQC (heteronuclear single quantum coherence) NMR analysis of PRshort indicates that cholic acid binds in the proposed PRshort dimerization interface and appears to impair formation of the correct dimer. NMR analysis by paramagnetic relaxation enhancement resulted in elevated transverse relaxation rates of those amino acids predicted to participate in dimer formation. Our results suggest transient PRshort homodimers are formed under native conditions but are only present as a minor transient species, which is not detectable by traditional methods.
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10

Golda, Mária, János András Mótyán, Mohamed Mahdi, and József Tőzsér. "Functional Study of the Retrotransposon-Derived Human PEG10 Protease." International Journal of Molecular Sciences 21, no. 7 (March 31, 2020): 2424. http://dx.doi.org/10.3390/ijms21072424.

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Paternally expressed gene 10 (PEG10) is a human retrotransposon-derived imprinted gene. The mRNA of PEG10 encodes two protein isoforms: the Gag-like protein (RF1PEG10) is coded by reading frame 1, while the Gag-Pol-like polyprotein (RF1/RF2PEG10) is coded by reading frames 1 and 2. The proteins are translated by a typical retroviral frameshift mechanism. The protease (PR) domain of RF2PEG10 contains an -Asp-Ser-Gly- sequence, which corresponds to the consensus -Asp-Ser/Thr-Gly- active-site motif of retroviral aspartic proteases. The function of the aspartic protease domain of RF2PEG10 remains unclear. To elucidate the function of PEG10 protease (PRPEG10), we designed a frameshift mutant (fsRF1/RF2PEG10) for comparison with the RF1/RF2PEG10 form. To study the effects of PRPEG10 on cellular proliferation and viability, mammalian HEK293T and HaCaT cells were transfected with plasmids coding for either RF1/RF2PEG10, the frameshift mutant (fsRF1/RF2PEG10), or a PR active-site (D370A) mutant fsRF1/RF2PEG10. Our results indicate that fsRF1/RF2PEG10 overexpression results in increased cellular proliferation. Remarkably, transfection with fsRF1/RF2PEG10 had a detrimental effect on cell viability. We hypothesize that PRPEG10 plays an important role in the function of this retroviral remnant, mediating the proliferation of cells and possibly implicating it in the inhibition of apoptosis.
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Більше джерел

Дисертації з теми "RETROVIRAL PROTEASE"

1

Peng, Kah Whye. "Protease-activatable targeted retroviral vectors." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624668.

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2

Garner, Joanne Clare. "Site directed mutagenesis, autoprocessing and inhibitor studies on the retroviral protease of the human immunodeficiency virus type-1." Thesis, University of Southampton, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302318.

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3

Muller, Natalie Guida. "Identificação de epitopos da protease de HIV-1 alvos de respostas de células T CD4+ em pacientes infectados pelo HIV-1." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/5/5146/tde-05032010-170301/.

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Introdução: Uma proporção significante de pacientes infectados por HIV-1 (pacientes HIV-1+) tratados com inibidores de protease (IPs) desenvolve mutações de resistência. Estudos recentes têm mostrado que células T CD8+ de pacientes HIV- 1+ reconhecem epitopos de Pol incluindo mutações selecionadas por drogas. Nenhum epitopo CD4+ da protease foi descrito na base de dados de Los Alamos. Objetivo: Considerando que a protease de HIV-1 é alvo de terapia antiretroviral e que essa pressão pode selecionar mutações, nós investigamos se mutações selecionadas por IPs afetariam o reconhecimento de epitopos da protease de HIV-1 por células T CD4+ em pacientes tratados com IPs. Nós investigamos o reconhecimento de três regiões da protease preditas de conter epitopos de células T CD4+ bem como mutações induzidas por IPs por células T CD4+ em pacientes HIV- 1+ tratados com IPs. Materiais e Métodos: Quarenta pacientes HIV-1+ tratados com IPs foram incluídos (30 em uso de Lopinavir/ritonavir, 9 em uso de Atazanavir/Ritonavir e 1 em uso exclusivo de Atazanavir). Para cada paciente determinou-se a seqüência endógena da protease de HIV-1, genotipagem viral e tipagem HLA classe II. Utilizamos o algoritmo TEPITOPE para selecionar peptídeos promíscuos, ligadores de múltiplas moléculas HLA-DR, codificando as três regiões da protease de HIV-1 cepa HXB2 (HXB2 4-23, 45-64, e 76-95) e 32 peptídeos adicionais contidos nas mesmas regiões incorporando as mutações induzidas por IPs mais freqüentes no Brasil. Os 35 peptídeos foram sintetizados. Respostas proliferativas de células T CD4+ e CD8+ aos peptídeos foram determinadas por ensaios de proliferação com diluição do corante CFSE. Ensaios de ligação a alelos HLA classe II foram realizados para confirmar a promiscuidade desses peptídeos e avaliar a habilidade de se ligarem a moléculas HLA presentes em cada paciente. Resultados: Todos os peptídeos foram reconhecidos por pelo menos um paciente e respostas proliferativas de células T CD4+ e CD8+ a pelo menos um peptídeo da protease de HIV-1 foram encontradas em 78% e 75% dos pacientes, respectivamente. A terceira região (Protease 76 95) foi a mais freqüentemente reconhecida. Ao compararmos as respostas de células T às seqüências da protease do HIV-1 endógeno, observamos que a maioria dos pacientes não foi capaz de reconhecer peptídeos idênticos às essas seqüências, porém reconheceram peptídeos variantes diferentes das mesmas regiões. Apenas sete pacientes responderam às seqüências endógenas. Verificamos que diversos peptídeos endógenos que não foram reconhecidos apresentaram ausência de ligação a alelos HLA portados por estes pacientes, sugerindo que mutações selecionadas por pressão imune tenham levado ao escape de apresentação de antígeno e evasão de resposta de linfócitos T CD4+. Alternativamente, isso poderia ser explicado pela presença de um vírus replicante distinto presente no plasma uma vez que somente foram obtidas seqüências provirais. Conclusão: Epitopos selvagens e mutantes da protease do HIV-1 reconhecidos por células T CD4+ foram identificados. Também verificamos que a maior parte dos pacientes não reconheceu as seqüências da protease endógena enquanto que reconheceram seqüências variantes. O reconhecimento de seqüências não-endógenas poderia ser hipoteticamente conseqüência de alvo de populações HIV-1 minoritárias; protease de HERV que contém regiões de similaridade com a protease do HIV-1; ou seqüências de HIV-1 presentes apenas em parceiros virêmicos. A falha de reconhecimento de seqüências endógenas seria mais provável devido ao escape imune, do que ao nível de apresentação ou reconhecimento por células T. Isso implica em uma conseqüência patofisiológica na evasão de respostas de células T contra a protease de HIV-1 e no fato de ser tradicionalmente considerada uma proteína pouco antigênica
Introduction: A significant proportion of protease inhibitor (PI)-treated HIV-1 infected (HIV-1+) patients develop resistance mutations. Recent studies have shown that CD8+ T cells from HIV-1 patients can recognize antiretroviral drug-induced mutant Pol epitopes. No HIV-1 protease CD4 epitopes are described in the Los Alamos database. Aims: Given that the protease of HIV-1 is a target of antiretroviral therapy and this pressure may lead to the selection of mutations, we investigated whether PI-induced mutations affect the recognition of HIV-1 protease epitopes by CD4 + T cells in PI-treated patients. We investigated the recognition of three protease regions predicted to harbor CD4+ T cell epitopes as well as PI-induced mutations by CD4+ T cells of PI-treated HIV-1+ patients. Methods: Forty PI-treated HIV-1+ patients were included (30 undergoing Lopinavir/ritonavir, 9 undergoing Atazanavir/ritonavir and 1 undergoing exclusively Atazanavir treatment). For each patients, the endogenous HIV-1 protease sequence, viral genotype and HLA class II typing were determined. We used the TEPITOPE algorithm to select promiscuous, multiple HLA-DR-binding peptides encoding 3 regions of HIV-1 HXB2 strain protease (HXB2 4-23, 45-64, and 76-95) and 32 additional peptides contained in the same regions, but encompassing the most frequent PI-induced mutations in Brazil. The 35 peptides were thus synthesized. Proliferative responses of CD4+ and CD8+ T cells against peptides were determined by the CFSE dilution assay. HLA class II binding assays were made to confirm the promiscuity of these peptides and evaluate their ability to bind the HLA molecules carried by each patient. Results: All tested peptides were recognized by at least one patient and proliferative responses of CD4+ and CD8+ T cells against at least one HIV-1 protease peptide were found in 78% and 75% patients, respectively. The third region (Protease 76-95) was the most frequently recognized. By comparing T-cell responses to HIV-1 endogenous protease sequences, we found that most patients failed to recognize identical peptides of those sequences, but recognized different variant peptides of the same region. Only seven patients responded to endogenous sequences. We found that several endogenous peptides that failed to be recognized showed no binding to the HLA alleles carried by that given patient, suggesting that mutations selected by immune pressure have led to escape of antigen presentation, as well as direct escape of the CD4+ T cell response. Alternatively, it could have been due to the presence of a different replicating virus in the plasma-since we only obtained proviral sequences. Conclusion: Wild-type and mutant HIV-1 protease epitopes recognized by CD4+ T cells were identified. We also found that most patients failed to recognize their endogenous protease sequences, while they recognized variant sequences. The recognition of non-endogenous sequences could hypothetically be a consequence of targeting a minor HIV-1 population; HERV protease, that contains regions of similarity with HIV-1 protease; or HIV-1 sequences present only in viremic partners. The failure to recognize endogenous sequences is most likely due to immune escape, either at the level of presentation or direct T cell recognition. This may have a pathophysiological consequence on evasion of T cell responses against protease and the fact that it has been considered traditionally a poorly antigenic HIV-1 protein.
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4

Junaid, Muhammad. "Studies of Retroviral Reverse Transcriptase and Flaviviral Protease Enzymes as Antiviral Drug Targets : Applications in Antiviral Drug Discovery & Therapy." Doctoral thesis, Uppsala universitet, Institutionen för farmaceutisk biovetenskap, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-173504.

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Viruses are a major threat to humans due to their unique adaptability, evolvability and  capability to control their hosts as parasites and genetic elements. HIV/AIDS is the third largest cause of death by infectious diseases in the world, and drug resistance due to the viral mutations is still the leading cause of treatment failure. The flaviviruses, such as Dengue virus (DEN) and Japanese encephalitis virus (JEV), represent other major cause of morbidity and mortality, and the areas where these viruses are endemic are spreading rapidly. No curative therapy for any flavivirus could be made available as yet. The first part of this thesis focuses on the HIV-1 drug resistance caused by mutations in a major HIV drug target, the HIV-1 reverse transcriptase (RT) as a response to the largest class of clinically used anti-retrovirals, the NRTIs. A robust proteochemometric model was created to analyse the complex mutation patterns in RT drug resistance. The model identified more than ten frequently-occurring mutations, each conferring at least two-fold decrease in susceptibility for one or several NRTIs. Using our prediction server (hivdrc.org), the model can be applied to propose optimum combination therapy for patients harbouring mutated HIV variants. The second part of the thesis encompasses studies on a promising drug target, the NS2B(H)-NS3pro, in two flaviviruses, namely the dengue virus (DEN) and Japanese encephalitis virus (JEV). Functional determinants of DEN NS2B(H)-NS3pro were identified by site-directed mutagenesis. Further, peptide inhibitors were designed using proteochemometrics (PCM) and statistical molecular design (SMD), synthesized and assayed on DEN proteases, which resulted in some novel peptides with low micromolar or sub-micromolar inhibitor activity. The very poorly characterised JEV NS2B(H)-NS3pro  was cloned, purified and the kinetic parameters of this attractive drug target were determined for a series of model substrates and inhibitor. The results identified the role in target-ligand interaction of different residues on specific positions in the target (NS2B(H)-NS3pro) and ligands (substrates/inhibitors). Overall, the findings in this thesis contribute to rational antiviral drug discovery and therapy.
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5

Hinks, John Andrew. "Studies of retroviral proteases." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1445580/.

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This work is primarily concerned with the expression, purification, and characterisation of aspartic proteases from three retroviruses of the lentivirus subgroup, specifically the Human Immunodeficiency Viruses types 1 and 2, and the Simian Immunodeficiency Virus isolated from the African Green Monkey (HIV-1 PR, HIV-2 PR, SIVagm PR respectively). These viruses cause immunodeficiency syndromes within their respective hosts, and understanding their molecular biology would facilitate development of Acquired Immunodeficiency Syndrome (AIDS) treatments in man. The proteases are essential to viral maturation and infection and are of great interest with respect to the development of new antivirals. This thesis describes attempts to develop improved methods for the over-expression and purification of these cytotoxic proteins for use in structural and biochemical studies. The development of a system for expression and purification of active, crystallisable HIV-1 PR is described, followed by a preliminary analysis of two compounds intended to act as irreversible "suicide inhibitors" of HIV-1 PR. The expression, purification, crystallisation, and preliminary crystallographic data for the native HIV-2 PR using the same expression system are also reported. Mutagenesis of the HIV-2 protease is described, whereby the conserved active site aspartic acids of the native homodimer were changed to histidine and cysteine, with the intention of modifying the enzyme's mechanism, whilst maintaining its native substrate specificity and overall structure. Finally the production of an insoluble, non-toxic, histidine tagged fusion of mutant E.coli Uracil DNA Glycosylase (UDG) and the SIVagm PR is reported. This was intended to produce high levels of a non-toxic fusion protein, allow one-step affinity purification, and provide native soluble protease following autocatalytic cleavage from the fusion protein. The effects of protease toxicity and codon usage on yields are discussed in light of the results presented.
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6

Leblanc, Pascal. "Retrovirus d'invertebres : zam un nouveau candidat chez drosophila melanogaster." Clermont-Ferrand 1, 1998. http://www.theses.fr/1998CLF1MM12.

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7

GESSNER, JEAN-YVES. "La proteine de la nucleocapside du retrovirus vih-1." Strasbourg 1, 1992. http://www.theses.fr/1992STR15031.

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8

Schucht, Roland. "Entwicklung von flexiblen Zelllinien für die Produktion rekombinanter Proteine und Retroviren." kostenfrei, 2006. http://www.digibib.tu-bs.de/?docid=00014003.

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9

Morphet, Marilynn Norma. "Method for identification of effective first-line treatment for HAART naïve HIV/AIDS patients." Thesis, Queensland University of Technology, 2002.

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Ménard, Armelle. "Purification, activité et inhibition de la protéase du rétrovirus BLV : un modèle d'étude pour celle du HTLV-1." Bordeaux 2, 1994. http://www.theses.fr/1993BOR28278.

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Книги з теми "RETROVIRAL PROTEASE"

1

Pearl, Laurence H., ed. Retroviral Proteases. London: Macmillan Education UK, 1990. http://dx.doi.org/10.1007/978-1-349-11907-3.

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1956-, Pearl Laurence H., and Medical Research Council (Great Britain). AIDS Directed Programme., eds. Retroviral proteases: Control of maturation and morphogenesis. New York, NY: Stockton Press, 1990.

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3

G, James Michael N., and International Conference on Aspartic Proteinases (7th : 1996 : Banff, Alta.), eds. Aspartic proteinases: Retroviral and cellular enzymes. New York: Plenum Press, 1998.

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1930-, Kostka Vladimír, and International Congress of Biochemistry (14th : 1988 : Prague, Czechoslovakia), eds. Proteases of retroviruses: Proceedings of the Colloquium C 52, 14th International Congress of Biochemistry, Prague, Czechoslovakia, July 10-15, 1988. Berlin: W. de Gruyter, 1989.

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5

Abelson, John N., Lawrence C. Kuo, Melvin I. Simon, and Jules A. Shafer. Retroviral Proteases. Elsevier Science & Technology Books, 1994.

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Retroviral Proteases: Control of Maturation and Morphogenesis. Macmillan Publishers Limited, 1990.

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(Editor), John N. Abelson, Melvin I. Simon (Editor), Lawrence C. Kuo (Editor), and Jules A. Shafer (Editor), eds. Retroviral Proteases, Volume 241 (Methods in Enzymology). Academic Press, 1994.

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8

Pearl, Laurence H. Retroviral Proteases: Control of Maturation and Morphogenesis. Stockton Pr, 1990.

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James, Michael N. G. Aspartic Proteinases: Retroviral and Cellular Enzymes. Springer, 2012.

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Aspartic Proteinases: Retroviral and Cellular Enzymes. Springer, 2011.

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Частини книг з теми "RETROVIRAL PROTEASE"

1

Yoshinaka, Yoshiyuki, Iyoko Katoh, and Kohei Oda. "Retroviral Protease: Substrate Specificity and Inhibitors." In Retroviral Proteases, 31–39. London: Macmillan Education UK, 1990. http://dx.doi.org/10.1007/978-1-349-11907-3_5.

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2

von der Helm, Klaus, S. Seelmeir, and U. Junker. "Characterisation and Inhibition of the Retroviral HIV-Protease." In Retroviral Proteases, 5–8. London: Macmillan Education UK, 1990. http://dx.doi.org/10.1007/978-1-349-11907-3_2.

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Wilderspin, Andrew, Duncan Gaskin, Risto Lapatto, Tom Blundell, Andrew Hemmings, John Overington, Jim Pitts, et al. "Three-dimensional Structure and Evolution of HIV-1 Protease." In Retroviral Proteases, 79–91. London: Macmillan Education UK, 1990. http://dx.doi.org/10.1007/978-1-349-11907-3_10.

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4

Debouck, Christine, Ingrid C. Deckman, Stephan K. Grant, Robert J. Craig, and Michael L. Moore. "The HIV-1 Aspartyl Protease: Maturation and Substrate Specificity." In Retroviral Proteases, 9–17. London: Macmillan Education UK, 1990. http://dx.doi.org/10.1007/978-1-349-11907-3_3.

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5

Roberts, M. M., and S. Oroszlan. "The Action of Retroviral Protease in Various Phases of Virus Replication." In Retroviral Proteases, 131–39. London: Macmillan Education UK, 1990. http://dx.doi.org/10.1007/978-1-349-11907-3_14.

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Miller, Maria, Amy L. Swain, Mariusz Jaskólski, Bangalore K. Sathyanarayana, Garland R. Marshall, Daniel Rich, Stephen B. H. Kent, and Alexander Wlodawer. "X-Ray Analysis of HIV-1 Protease and Its Complexes with Inhibitors." In Retroviral Proteases, 93–106. London: Macmillan Education UK, 1990. http://dx.doi.org/10.1007/978-1-349-11907-3_11.

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Singh, O. M. P., E. M. J. Roud Mayne, and M. P. Weir. "Dimerisation of the HIV-1 Protease: Preliminary Analysis Using Gel Permeation Chromatography." In Retroviral Proteases, 73–78. London: Macmillan Education UK, 1990. http://dx.doi.org/10.1007/978-1-349-11907-3_9.

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Moelling, K., M. Nawrath, T. Schulze, L. Pavlitzkova, M. Soucek, K. H. Budt, L. H. Pearl, M. T. Knoop, J. Kay, and V. Kruft. "Cleavage of RT/RNase H by HIV-1 Protease and Analysis of Substrate Cleavage Sites in vitro." In Retroviral Proteases, 19–29. London: Macmillan Education UK, 1990. http://dx.doi.org/10.1007/978-1-349-11907-3_4.

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Matsui, Takeshi. "Endogenous Retroviral-Like Aspartic Protease, SASPase as a Key Modulator of Skin Moisturization." In Treatment of Dry Skin Syndrome, 179–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-27606-4_12.

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Pearl, Laurence H. "Introduction." In Retroviral Proteases, 1–3. London: Macmillan Education UK, 1990. http://dx.doi.org/10.1007/978-1-349-11907-3_1.

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Звіти організацій з теми "RETROVIRAL PROTEASE"

1

Paulovich, Amanda, Biing Y. Lin, and Kyle J. Garton. Identification of Breast Cancer Serum Biomarkers: A Novel Retroviral Library Screen to Define the Breast Cancer-Soluble Ectodomain Proteome. Fort Belvoir, VA: Defense Technical Information Center, October 2009. http://dx.doi.org/10.21236/ada515795.

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