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trans activation of gene expression by v-myb
1Department of Pathology, University of California, San Diego School of Medicine, La Jolla 92093.
Molecular and Cellular Biology
|May 1, 1990
Summary
The v-myb oncogene product, p48v-myb, transforms myeloid cells and activates gene expression. DNA binding alone may not be sufficient for this transactivation function.
Area of Science:
- Molecular Biology
- Oncology
- Virology
Background:
- The v-myb oncogene induces acute myeloid leukemia in chickens.
- Its protein product, p48v-myb, is a nuclear protein that binds DNA and transforms myeloid cells.
- Understanding the function of p48v-myb is crucial for leukemia research.
Purpose of the Study:
- To investigate the transactivation potential of p48v-myb.
- To identify the domains of p48v-myb required for transactivation and transformation.
- To explore the relationship between DNA binding and transactivation by p48v-myb.
Main Methods:
- Transient DNA transfection assays were used to assess gene expression.
- Mutational analysis identified key domains of p48v-myb.
- Reporter gene assays with herpes simplex virus thymidine kinase promoter were employed.
Main Results:
- p48v-myb functions as a transactivator of gene expression.
- Both the amino-terminal DNA-binding domain and the carboxyl-terminal domain are essential for transformation and transactivation.
- While p48v-myb binds DNA, its binding to consensus sequences upstream of a promoter did not lead to transcriptional activation, unlike a v-myb-VP16 fusion protein.
Conclusions:
- p48v-myb possesses transactivation capabilities essential for myeloid cell transformation.
- Specific domains of p48v-myb are critical for its oncogenic function.
- DNA binding by p48v-myb may not be sufficient for transcriptional activation, suggesting additional regulatory mechanisms are involved.