References of "Kettmann, Richard"
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See detailBovine Leukemia Virus Su Protein Interacts With Zinc, And Mutations Within Two Interacting Regions Differentially Affect Viral Fusion And Infectivity In Vivo
Gatot, Js.; Callebaut, I.; Van Lint, C. et al

in Journal of Virology (2002), 76(16),

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See detailSubcellular Localization Of The Bovine Leukemia Virus R3 And G4 Accessory Proteins
Lefebvre, Laurent; Ciminale, Vincenzo; Vanderplasschen, Alain ULg et al

in Journal of Virology (2002), 76(15), 7843-7854

Bovine leukemia virus (BLV) is a complex retrovirus that belongs to the Deltaretrovirus genus, which also includes Human T-cell leukemia virus type 1 (HTLV-1). Both viruses contain an X region coding for ... [more ▼]

Bovine leukemia virus (BLV) is a complex retrovirus that belongs to the Deltaretrovirus genus, which also includes Human T-cell leukemia virus type 1 (HTLV-1). Both viruses contain an X region coding for at least four proteins: Tax and Rex, which are involved in transcriptional and posttranscriptional regulation, respectively, and the accessory proteins R3 and G4 (for BLV) and p12(I), p13(II), and p30(II) (for HTLV-1). The present study was aimed at characterizing the subcellular localization of BLV R3 and G4. The results of immunofluorescence experiments on transfected HeLa Tat cells demonstrated that R3 is located in the nucleus and in cellular membranes, as previously reported for HTLV-1 p12(1). In contrast, G4, like p13(II), is localized both in the nucleus and in mitochondria. In addition, we have shown that G4 harbors a mitochondrial targeting signal consisting of a hydrophobic region and an amphipathic alpha-helix. Thus, despite a lack of significant primary sequence homology, R3 and p12(1) and G4 and p13(II) exhibit similar targeting properties, suggesting possible overlap in their functional properties. [less ▲]

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See detailInhibition Of Histone Deacetylases Induces Bovine Leukemia Virus Expression In Vitro And In Vivo
Merezak, C.; Reichert, M.; Van Lint, C. et al

in Journal of Virology (2002), 76(10),

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See detailIncreased Cell Proliferation, But Not Reduced Cell Death, Induces Lymphocytosis In Bovine Leukemia Virus-Infected Sheep
Debacq, C.; Asquith, B.; Kerkhofs, P. et al

in Proceedings of the National Academy of Sciences of the United States of America (2002), 99(15),

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See detailCell turnover in BLV-infected sheep
Debacq, Christophe; Peremans, T.; Kerkhofs, Pierre et al

in Aids Research and Human Retroviruses": 10th International Conference on Human Retrovirology: HTLV and Related Viruses, (2001, June)

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See detailA critical cysteine residue of bovine leukemia virus SU protein interacts with zinc and plays a role in viral infectivity.
Gatot, Jean-Stéphane; Kerkhofs, Pierre; Burny, Arsène et al

in The 2001 meeting on Retroviruses. (2001, May)

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See detailCell turnover in BLV-infected sheep.
Debacq, C.; Peremans, T.; Kerkhofs, P. et al

in AIDS Research and Human Retroviruses (2001), 17(1), 13

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See detailSuboptimal Enhancer Sequences Are Required For Efficient Bovine Leukemia Virus Propagation In Vivo: Implications For Viral Latency
Merezak, C.; Pierreux, C.; Adam, E. et al

in Journal of Virology (2001), 75(15),

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See detailRole Of The Proline-Rich Motif Of Bovine Leukemia Virus Transmembrane Protein Gp30 In Viral Load And Pathogenicity In Sheep
Reichert, M.; Winnicka, A.; Willems, Luc ULg et al

in Journal of Virology (2001), 75(17),

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See detailGenetic Determinants Of Bovine Leukemia Virus Pathogenesis
Willems, Luc ULg; Burny, A.; Collete, Delphine et al

in Aids Research and Human Retroviruses (2000), 16(16), 1787-95

The understanding of HTLV-induced disease is hampered by the lack of a suitable animal model allowing the study of both viral replication and leukemogenesis in vivo. Although valuable information has been ... [more ▼]

The understanding of HTLV-induced disease is hampered by the lack of a suitable animal model allowing the study of both viral replication and leukemogenesis in vivo. Although valuable information has been obtained in different species, such as rabbits, mice, rats, and monkeys, none of these systems was able to conciliate topics as different as viral infectivity, propagation within the host, and generation of leukemic cells. An alternate strategy is based on the understanding of diseases induced by viruses closely related to HTLV-1, like bovine leukemia virus (BLV). Both viruses indeed belong to the same subfamily of retroviruses, harbor a similar genomic organization, and infect and transform cells of the hematopoietic system. The main advantage of the BLV system is that it allows direct experimentation in two different species, cattle and sheep. [less ▲]

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See detailDiscordance between bovine leukemia virus tax immortalization in vitro and oncogenicity in vivo.
Twizere, Jean-Claude ULg; Kerkhofs, Pierre; Burny, Arsène et al

in Journal of Virology (2000), 74(21), 9895-902

Bovine leukemia virus (BLV) Tax protein, a transcriptional activator of viral expression, is essential for viral replication in vivo. Tax is believed to be involved in leukemogenesis because of its second ... [more ▼]

Bovine leukemia virus (BLV) Tax protein, a transcriptional activator of viral expression, is essential for viral replication in vivo. Tax is believed to be involved in leukemogenesis because of its second function, immortalization of primary cells in vitro. These activities of Tax can be dissociated on the basis of point mutations within specific regions of the protein. For example, mutation of the phosphorylation sites at serines 106 and 293 abrogates immortalization potential in vitro but maintains transcriptional activity. This type of mutant is thus particularly useful for unraveling the role of Tax immortalization activity during leukemogenesis independently of viral replication. In this report, we describe the biological properties of BLV recombinant proviruses mutated in the Tax phosphorylation sites (BLVTax106+293). Titration of the proviral loads by semiquantitative PCR revealed that the BLV mutants propagated at wild-type levels in vivo. Furthermore, two animals (sheep 480 and 296) infected with BLVTax106+293 developed leukemia or lymphosarcoma after 16 and 36 months, respectively. These periods of time are within the normal range of latencies preceding the onset of pathogenesis induced by wild-type viruses. The phenotype of the mutant-infected cells was characteristic of a B lymphocyte (immunoglobulin M positive) expressing CD11b and CD5 (except at the final stage for the latter marker), a pattern that is typical of wild-type virus-infected target cells. Interestingly, the transformed B lymphocytes from sheep 480 also coexpressed the CD8 marker, a phenotype rarely observed in tumor biopsies from chronic lymphocytic leukemia patients. Finally, direct sequencing of the tax gene demonstrated that the leukemic cells did not harbor revertant proviruses. We conclude that viruses expressing a Tax mutant unable to transform primary cells in culture are still pathogenic in the sheep animal model. Our data thus provide a clear example of the discordant conclusions that can be drawn from in vitro immortalization assays and in vivo experiments. These observations could be of interest for other systems, such as the related human T-cell leukemia virus type 1, which currently lack animal models allowing the study of the leukemogenic process. [less ▲]

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See detailProtective Effects Of A Live Attenuated Bovine Leukaemia Virus Vaccine With Deletion In The R3 And G4 Genes
Reichert, M.; Cantor, Gh.; Willems, Luc ULg et al

in Journal of General Virology (2000), 81

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See detailLong-Term Protection Against Bovine Leukaemia Virus Replication In Cattle And Sheep
Kerkhofs, P.; Gatot, Js.; Knapen, K. et al

in Journal of General Virology (2000), 81

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See detailImplication de la protéine transmembranaire d’enveloppe du virus de la leucémie bovine dans la fusion cellulaire et l’infectivité virale.
Gatot, Jean-Stéphane; Callebaut, Isabelle; Mornon, Jean-Paul et al

in Séminaire de la Recherche Télévie (1999, March 16)

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See detailBovine leukemia virus as a model for human T-cell leukemia virus
Willems, Luc ULg; Burny, A.; Dangoisse, O. et al

in Current Topics in Virology (1999)

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See detailBovine Leukemia Virus-Induced Persistent Lymphocytosis In Cattle Does Not Correlate With Increased Ex Vivo Survival Of B Lymphocytes
Dequiedt, Franck ULg; Cantor, Gh.; Hamilton, Vt. et al

in Journal of Virology (1999), 73(2),

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See detailTranscriptional Regulation Of The Mn/Ca 9 Gene Coding For The Tumor-Associated Carbonic Anhydrase Ix - Identification And Characterization Of A Proximal Silencer Element
Kaluz, S.; Kaluzova, M.; Opavsky, R. et al

in Journal of Biological Chemistry (1999), 274(46),

The MN/CA 9 (MN) gene encodes a tumor-associated isoenzyme of the carbonic anhydrase family. Functional characterization of the 3. 5-kilobase pair MN 5' upstream region by deletion analysis led to the ... [more ▼]

The MN/CA 9 (MN) gene encodes a tumor-associated isoenzyme of the carbonic anhydrase family. Functional characterization of the 3. 5-kilobase pair MN 5' upstream region by deletion analysis led to the identification of the -173 to +31 fragment as the MN promoter. In vitro DNase I footprinting revealed the presence of five protected regions (PRs) within the MN promoter. Detailed deletion analysis of the promoter identified PR1 and PR2 (numbered from the transcription start) as the most critical for transcriptional activity. PR4 negatively affected transcription, since its deletion led to increased promoter activity and was confirmed to function as a promoter-, position-, and orientation-independent silencer element. Mutational analysis indicated that the direct repeat AGGGCacAGGGC is required for efficient repressor binding. Two components of the repressor complex (35 and 42 kDa) were found to be in direct contact with PR4 by UV cross-linking. Increased cell density, known to induce MN expression, did not affect levels of PR4 binding in HeLa cells. Significantly reduced repressor level seems to be responsible for MN up-regulation in the case of tumorigenic CGL3 as compared with nontumorigenic CGL1 HeLa x normal fibroblast hybrid cells. [less ▲]

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See detailLeukemia Viruses
Burny, A.; Bex, F.; Dequiedt, Franck ULg et al

in Encyclopedia of Immunology, Academic Press (1998)

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