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J Biol Chem, Vol. 273, Issue 12, 6878-6884, March 20, 1998
From the Section on Growth Factors, NICHD and the ¶ Laboratory
of Molecular Biology, Division of Basic Sciences, NCI, National
Institutes of Health, Bethesda, Maryland 20892
Treatment of PC12 cells with nerve growth factor
leads to a decrease in the number of epidermal growth factor receptors
on the cell membrane. The mRNA for the epidermal growth factor
receptor decreases in a comparable fashion. This decrease appears due
to a decrease in the transcription of the epidermal growth factor receptor gene because first, there is no difference in the stability of
the epidermal growth factor receptor mRNA, second, newly
transcribed epidermal growth factor receptor mRNA is decreased in
nerve growth factor-differentiated cells, and third, constructs
containing the promoter region of the epidermal growth factor receptor
gene are transcribed much less readily in nerve growth
factor-differentiated cells than in untreated cells. The decreases in
mRNA are not seen in the p140trk-deficient variant PC12nnr5
cells nor in cells containing either dominant-negative Ras or
dominant-negative Src. Treatment with nerve growth factor also
increases the cellular content of GCF2, a putative transcription factor
inhibitory for the transcription of the epidermal growth factor
receptor gene. The increase in GCF2, like the decrease in the epidermal
growth factor receptor mRNA, is not seen in PC12nnr5 cells nor in
cells expressing either dominant-negative Ras or dominant-negative Src.
The results suggest that nerve growth factor-induced down-regulation of
the epidermal growth factor receptor is under transcriptional control,
is p140trk-, Ras-, and Src-dependent, and may
involve transcriptional repression by GCF2.
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