Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-2-22
pubmed:abstractText
Mutations in the tumour suppressor gene l(2)gl cause formation of brain and imaginal disc tumours. The product of this gene was suggested to be a part of an intercellular communication system, regulating cell growth and differentiation. Oncogenic activation of many signalling pathways, involved in similar processes, result in increased activity of the AP-1 family of transcription factors. In this paper we explored the interaction between the cancer mutation l(2)gl and the level of transcription of the AP-1 proteins. We report that in brain tumours from l(2)gl-deficient larvae, transcription of the Drosophila melanogaster c-fos homologue was stimulated but that of the c-jun homologue was unchanged. Our results provide further evidence that the protein l(2)gl is a component of a signalling pathway, a nuclear target of which is the AP-1 family of transcription factors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1357-2725
pubmed:author
pubmed:issnType
Print
pubmed:volume
33
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
45-51
pubmed:dateRevised
2006-5-1
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Transcription of Dfos is stimulated by brain tumours of l(2)gl-deficient larvae of Drosophila melanogaster.
pubmed:affiliation
Department of Genetics, Faculty of Biology, University of Sofia, 8 Dragan Tsankov Str., 1421 Sofia, Bulgaria.
pubmed:publicationType
Journal Article