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.
Statistical Data Included, Genetic aspects, Non-Hodgkin's lymphomas, Cell cycle

User Contributions:

Comment about this article or add new information about this topic:

CAPTCHA

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.
DNA damage, Cellular signal transduction, RNA splicing

User Contributions:

Comment about this article or add new information about this topic:

CAPTCHA

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
Papillomaviruses, Papillomavirus, Antiviral agents, Antiviral agent structure-activity relationships

User Contributions:

Comment about this article or add new information about this topic:

CAPTCHA


subjects list: Research, United States, Physiological aspects, Cell death, Genetic transcription, Transcription (Genetics), Cytochemistry, Interferon
This website is not affiliated with document authors or copyright owners. This page is provided for informational purposes only. Unintentional errors are possible.