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v-Src and EJ Ras alleviate repression of c-Jun by a cell-specific inhibitor
V R Baichwal1, A Park, R Tjian
1Howard Hughes Medical Institute, University of California, Berkeley 94720.
Nature
|July 11, 1991
Summary
Proto-oncogenes like src and ras activate the transcription factor AP-1 (activator protein-1) by disrupting its inhibitor. This oncogene-induced AP-1 activity is mediated by the c-Jun activation domain.
Area of Science:
- Molecular biology
- Cellular signaling
- Cancer research
Background:
- The AP-1 family of transcription factors, including c-Jun and c-Fos, regulates cellular genes and oncogene expression.
- c-Jun transcriptional activity is inhibited by a cell-type-specific inhibitor acting on its activation domain (A1) and negative regulatory region (delta).
Purpose of the Study:
- To investigate the mechanism by which src and ras oncogenes enhance c-Jun transcriptional activity.
- To identify the specific region of c-Jun involved in oncogene-mediated stimulation.
Main Methods:
- Cotransfection of src or ras oncogenes with a GAL4:c-Jun hybrid construct.
- Assessing transcriptional activity in cell lines with and without the c-Jun inhibitor.
Main Results:
- Src and ras oncogenes enhance the transcriptional activity of a GAL4:c-Jun hybrid containing the delta-A1 region, independent of c-Jun's DNA binding and dimerization domains.
- Oncogene-induced c-Jun activity is observed in cells with the inhibitor but not in cells lacking it.
- The A1 domain of c-Jun is essential for stimulation by src and ras.
Conclusions:
- Src and ras oncogenes stimulate c-Jun and AP-1 transcriptional activity.
- This stimulation likely occurs through signal-transduction pathways that disrupt the interaction between c-Jun and its inhibitor.
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