Communications publiées lors de congrès ou colloques nationaux et internationaux (118)
100.
Kiermer, V., Dequiedt, F., Van Lint, C., Verdin, E., Burny, A., & Droogmans, L. (1996). The role of a potential c-Myc/Max binding site on the bovine leukemia virus long terminal repeat transcriptional activity. Abstract of the 8th workshop on Pathogenesis of Animal Retroviruses (23-25 Oct, 1996: Saint-Malo, France)101.
Van Lint, C., Amella, C. A., John, M., Jie, T., Emiliani, S., & Verdin, E. (1996). A new enhancer downstream of the transcription start site of HIV-1 is critical for virus infectivity. Abstract of the Retroviruses Meeting (21-26 May, 1996: Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, USA)102.
Verdin, E., Van Lint, C., Emiliani, S., & Ott, M. (1996). Chromatin is an integral component of HIV-1 transcriptional repression and activation. Abstract of the Keystone Symposium on Molecular and Cellular Biology "Molecular Biology of HIV" (17-23 Jan, 1996: Taos, New Mexico, USA)103.
Ott, M., Emiliani, S., Van Lint, C., Herbein, G., Chirmule, N., Lovett, J., Mc Closkey, T., Pahwa, S., & Verdin, E. (1996). The HIV Tat protein confers hypersensitivity to CD28-mediated costimulatory signals in infected T cells. ). Abstract of the 1996 Annual Meeting of the Institute of Human Virology (7-13 Sept, 1996: Baltimore, Maryland)104.
Kiermer, V., Van Lint, C., Verdin, E., Burny, A., & Droogmans, L. (1996). The role of the RU5 region of the Bovine leukemia virus genome in the transcriptional control of viral expression. Achives Internationales de Physiologie, de Biochimie et de Biophysique (1996: Société Belge de Biochimie, Brussels, Belgium)105.
Van Lint, C., Ghysdael, J., Vanhulle, C., Paras, P., Burny, A., & Verdin, E. (1995). A transcriptional regulatory element is associated with a nuclease-hypersensitive site in the pol gene of HIV-1. Abstract of the Baxter Nobel Symposium on "Molecular design for life" (12 Janv 1995: Brussels, Belgium)106.
Van Lint, C., Ott, M., Emiliani, S., Jie, T., & Verdin, E. (1995). Histone hyperacetylation induces HIV-1 gene expression in latently infected cell lines. Abstract of the Retroviruses Meeting (23-28 May, 1995: Cold Spring Harbor, New York, USA)108.
Van Lint, C., Emiliani, S., Ott, M., & Verdin, E. (1995). Histone hyperacetylation causes the disruption of a single nucleosome in the HIV-1 promoter and transcriptional activation. Abstract of the Fourteenth Summer Symposium in Molecular Biology "Chromosomal Controls of Gene Expression" (3-5 Aug, 1995: The Pennsylvania State University, Pennsylvania, USA)109.
Van Lint, C., Emiliani, S., Ott, M., & Verdin, E. (1995). Histone hyperacetylation causes the disruption of a single nucleosome in the HIV-1 promoter and transcriptional activation. Abstract of the Cold Spring Harbor Meeting on Cancer Cells "Mechanisms of Eukaryotic Transcription" (30 Aug-3 Sept, 1995: Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, USA)110.
Emiliani, S., Ott, M., Van Lint, C., Jie, T., & Verdin, E. (1995). Mechanism of HIV-1 latency: a mutation in the TAR region impairs Tat responsiveness of the promoter and is complemented by TNF-a/TPA treatment. Abstract of the Retroviruses Meeting (23-28 May, 1995: Cold Spring Harbor, New York, USA)111.
Van Lint, C., Ghysdael, J., Vanhulle, C., Paras, P., Burny, A., & Verdin, E. (1994). A transcriptional regulatory region is associated with a nuclease hypersensitive site in the pol gene of HIV-1 in a promonocytic cell line. Abstract of the Annual Meeting of the N.I.H. Laboratory of Tumor Cell Biology (25 Sept - 1 Oct, 1994: Bethesda, Maryland, USA)