Linked Life Data

2150599

Source:http://linkedlifedata.com/resource/pubmed/id/2150599

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1991-5-16
pubmed:abstractText
The Mos protein is a serine/threonine protein kinase that is likely to be a part of signal transduction pathways that regulate cell growth. We show here that expression of the v-Mos protein leads to a transient transcriptional activation of the c-fos and the c-jun proto-oncogenes in NIH 3T3 cells. Different cis-acting promoter elements are responsible for this effect. In the c-fos promoter the dyad symmetry element (DSE, also known as serum response element, SRE) is sufficient to confer responsiveness to the v-Mos protein. In the c-jun promoter the 12-0-tetradecanoyl-phorbol-13-acetate (TPA) response element (TRE) mediates this effect. Various Mos mutants with decreased transforming activity have diminished trans-acting activity on the c-fos and c-jun promoters. These results suggest that the highly transforming v-Mos protein exerts at least some of its effects through the induction of expression of the c-fos and c-jun protooncogenes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1043-4674
pubmed:author
pubmed:issnType
Print
pubmed:volume
2
pubmed:geneSymbol
c-fos, c-jun, v-mos
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
143-50
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Different promoter elements are required for the induced expression of c-fos and c-jun proto-oncogenes by the v-mos oncogene product.
pubmed:affiliation
Department of Medicine, University of California, San Diego, La Jolla 92093.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't