Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1993-3-26
pubmed:abstractText
The present work demonstrates that ethanol induces expression of the c-jun proto-oncogene in human keratinocytes. Increased c-jun mRNA levels were detectable at 1 hr of exposure to 1% ethanol and at 24 hr remained above that in control keratinocytes. An increase in c-jun expression was also detectable at ethanol concentrations of 0.1 and 0.5%. Similar findings were obtained for the related jun-B and c-fos early response genes. The results also demonstrate that ethanol exposure is associated with increases in protein kinase C activity in both the cytosol and membrane fractions. This increase was detectable at 5 min and maximal at 30-60 min. The finding that induction of c-jun expression by ethanol was inhibited by the isoquinolinesulfonamide derivative H7, but not by HA1004, suggested that this effect is mediated by protein kinase C. Furthermore, down-regulation of protein kinase C by prolonged exposure to 12-O-tetradecanoylphorbol-13-acetate was associated with a block in ethanol-induced c-jun expression. We also demonstrated that ethanol exposure is associated with rapid (5-30 min) increases in intracellular levels of diradylglycerol. Taken together, these findings demonstrate that the exposure of keratinocytes to ethanol results in the activation of protein kinase C and c-jun expression.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0006-2952
pubmed:author
pubmed:issnType
Print
pubmed:day
9
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
675-81
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Induction of the c-jun proto-oncogene by a protein kinase C-dependent mechanism during exposure of human epidermal keratinocytes to ethanol.
pubmed:affiliation
Laboratory of Clinical Pharmacology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't