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(Received for publication, April 10, 1995; and in revised form, May 19, 1995) From the We previously found that the level of Fas, a cell surface
receptor for an apoptosis signal, increases at the mRNA level in
influenza virus-infected HeLa cells prior to their death by apoptosis.
Here we investigated the mechanism of activation of the Fas-encoding
gene expression upon influenza virus infection. Nucleotide sequences
for the binding of nuclear factor for interleukin-6 expression
(NF-IL6), also known as CCAAT/enhancer-binding protein
Volume 270,
Number 30,
Issue of July 28, pp. 18007-18012, 1995
©1995 by The American Society for Biochemistry and Molecular Biology, Inc.
, were
repeated 8 times in the 5`-end region of the human FAS gene,
spanning from -1360 to +320. This region directed the
expression of a downstream marker gene when introduced into HeLa cells
and the activity of the FAS gene promoter was stimulated about
2-fold upon influenza virus infection. Gene expression driven by the FAS promoter was activated when human NF-IL6 was overproduced
in a DNA co-transfection study. Moreover, the DNA-binding activity of
NF-IL6 increased after infection with the virus, whereas the amount of
NF-IL6 seemed unchanged. The results suggest that NF-IL6 is activated
upon influenza virus infection through post-translational modification
and that the modified factor stimulates the transcription of the human FAS gene.
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