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Vol. 62, Issue 2, 272-280, August 2002
Ernest Gallo Research Center, Emeryville, California (D.-Y.H.,
A.J.V., R.Y., D.R.); and Department of Neurology, University of
California, San Francisco, California (D.R.)
Scaffolding proteins such as receptor for activated C kinase (RACK) 1 are involved in the targeting of signaling proteins and play an
important role in the regulation of signal transduction cascades. Recently, we found that in cultured cells and in vivo, acute ethanol exposure induces the nuclear compartmentalization of
RACK1. To elucidate a physiological role for nuclear RACK1, the Tat
protein transduction system was used to transduce RACK1 and
RACK1-derived fragments into C6 glioma cells. We found that nuclear
RACK1 is mediating the induction of the immediate early gene
c-fos expression induced by ethanol. First, transduction of full-length RACK1 (Tat-RACK1) resulted in the induction of c-fos expression and enhancement of ethanol activities.
Second, we determined that the C terminus of RACK1 (Tat-RACK1
N) is
mediating transcription. Third, we identified a dominant negative
fragment of RACK1 that inhibited the nuclear compartmentalization of
endogenous RACK1 and inhibited ethanol-induction of c-fos mRNA and
protein expression. Last, acute exposure to ethanol or transduction of full-length Tat-RACK1 resulted in an increase in mRNA levels of an
activator protein 1 site-containing gene, PAC1
(pituitary adenylate cyclase-activating polypeptide receptor type I),
suggesting that nuclear RACK1 is involved in the regulation of the
expression of genes that are altered upon acute ethanol treatment.
These results may therefore have important implications for the study of alcohol addiction.
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