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Glutaredoxin is a direct target of oncogenic jun
M E Goller1, J S Iacovoni, P K Vogt
1The Scripps Research Institute, Department of Molecular and Experimental Medicine, La Jolla, California 92037, USA.
Abstract:
We have analysed differential gene expression in v-jun-transformed chicken embryo fibroblasts (CEF) compared to normal CEF by using the directional tag PCR subtraction method. From a first generation of putative Jun targets four clones were selected for study; they are upregulated in jun-transformed cells. Three of these clones showed homology to known genes: glutaredoxin, growth associated protein (GAP)-43/neuromodulin, and phenobarbital-induced cytochrome P450. The expression of these genes was analysed in fibroblasts transformed by various oncogenes. Expression of the glutaredoxin mRNA could be induced by a Jun-estrogen receptor chimaera in the absence of de novo protein biosynthesis. Based on this observation we conclude that glutaredoxin is a direct target of v-Jun.
Insights
Researchers identified glutaredoxin as a direct target of v-Jun in chicken embryo fibroblasts (CEF). This finding advances understanding of gene regulation in oncogenic transformation and cellular growth.
Area of Science:
- Molecular Biology
- Oncology
- Cell Biology
Background:
- Oncogenic transformation by viral Jun (v-Jun) alters gene expression profiles in chicken embryo fibroblasts (CEF).
- Identifying direct transcriptional targets of v-Jun is crucial for understanding its oncogenic mechanisms.
Purpose of the Study:
- To identify and characterize novel genes directly regulated by v-Jun in CEF.
- To investigate the role of identified target genes in oncogenic transformation.
Main Methods:
- Differential gene expression analysis using directional tag PCR subtraction.
- Cloning and sequencing of upregulated genes.
- Expression analysis in fibroblasts transformed by various oncogenes.
- Induction of gene expression using a v-Jun-estrogen receptor chimera.
Main Results:
- Four putative v-Jun target genes were identified, with three showing homology to known genes: glutaredoxin, growth-associated protein (GAP)-43/neuromodulin, and phenobarbital-induced cytochrome P450.
- Glutaredoxin mRNA expression was inducible by a v-Jun-estrogen receptor chimera, independent of new protein synthesis.
- Expression patterns of these genes were analyzed in fibroblasts transformed by different oncogenes.
Conclusions:
- Glutaredoxin is identified as a direct transcriptional target of v-Jun.
- The findings provide insights into the molecular mechanisms of v-Jun-mediated oncogenesis.
- Glutaredoxin's role in cellular transformation warrants further investigation.