Control of beta-interferon expression in murine embryonal carcinoma F9 cells.
AUTOR(ES)
Francis, M K
RESUMO
Murine embryonal carcinoma F9 cells, a tissue culture model for early embryonic development, do not produce interferon (IFN) in response to poly(I-C), as determined by an antiviral assay. RNase protection analyses were used to examine total RNA extracted from the cells for the presence of beta-IFN RNA. Whereas F9 cells differentiated in vitro with retinoic acid produced a biologically active protein as well as beta-IFN RNA in response to poly(I-C), undifferentiated F9 cells produced no detectable beta-IFN RNA even in the presence of cycloheximide, an IFN-superinducing agent. These results show that undifferentiated embryonal carcinoma cells do not accumulate beta-IFN RNA in response to an IFN-inducing agent, suggesting a transcriptional regulatory mechanism. However, this control mechanism is altered upon differentiation, since the gene can be transcriptionally activated in retinoic acid-differentiated cells.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=362405Documentos Relacionados
- NF-kappa B-independent activation of beta-interferon expression in mouse F9 embryonal carcinoma cells.
- Retroviral vector gene expression in F9 embryonal carcinoma cells.
- SNF2beta-BRG1 is essential for the viability of F9 murine embryonal carcinoma cells.
- Two levels of regulation of beta-interferon gene expression in human cells.
- Regulated expression of an extrachromosomal human beta-interferon gene in mouse cells.