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BCoR, a novel corepressor involved in BCL-6 repression

Article Abstract:

A novel BCL-6 interacting corepressor, BCoR, has been identified, characterized, and found to be involved in BCL-6 repression and perhaps BCL-6-associated lymphomas. BCoR can act as a corepressor when tethered to DNA and can potentiate BCL-6 repression when overexpressed. Certain class I and II histone deacetylases (HDACs) interact in vivo with BCoR. This indicates that BCoR may interact selectively with the POZ domain of BCL-6, but not with eight additional POZ proteins tested, PLZF included.

Author: Fischle, Wolfgang, Verdin, Eric, Huynh, Khanh D., Bardwell, Vivian J.
Publisher: Cold Spring Harbor Laboratory Press
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 2000
Statistical Data Included, Genetic aspects, Non-Hodgkin's lymphomas, Cell cycle

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Dual utilization of an acceptor/donor splice site governs the alternative splicing of the IRF-3 gene

Article Abstract:

Dual use of an acceptor/donor splice site has been found to govern alternative splicing of the interferon regulatory factor-3 (IRF-3) gene. The alternative spice isoform, IRF-3a, encoded by the IRF-3 gene is expressed in all tissues and cell lines tested. Ratios of IRF-3a to IRF3 mRNA are varied. Sequences downstream from the unusual splice junction can bind members of the ST protein family. This can affect splice site selection.

Author: Karpova, Alla Y., Howley, Peter M., Ronco, Lucienne V.
Publisher: Cold Spring Harbor Laboratory Press
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 2000
DNA damage, Cellular signal transduction, RNA splicing

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Human papillomavirus 16 E6 oncoprotein binds to interferon regulatory factor-3 and inhibits its transcriptional activity

Article Abstract:

Studies show the binding of human papillomavirus 16 E6 (HPV16 E6) to interferon regulatory factor-3 (IRF-3) prevents the interferon's transcriptional activity. This binding process does not create degradation or ubiquitination of HPV16 E6, and by inhibiting IRF-3's transcriptional activity, HPV16 E6 may be able to circumvent antiviral cellular response.

Author: Karpova, Alla Y., Howley, Peter M., Ronco, Lucienne V., Vidal, Marc
Publisher: Cold Spring Harbor Laboratory Press
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 1998
Papillomaviruses, Papillomavirus, Antiviral agents, Antiviral agent structure-activity relationships

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Subjects list: Research, United States, Physiological aspects, Cell death, Genetic transcription, Transcription (Genetics), Cytochemistry, Interferon
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