The cellular oncogene, c-myc, has been found to be activated in a wide range of cancer cells by chromosomal translocation, gene amplification and proviral integration. The focus of this proposal will be to understand the function of the c-myc protein in controlling normal and tumor cell growth. The specific goals of the proposal are as follows: 1. The c-myc protein complex isolated from normal and myc-transformed cells will be investigated to characterize associated proteins. 2. The role of phosphorlylation in controlling the DNA binding activity and/or specificity of Max and Myc will be investigated through structure function studies. In particular, we will analyze a domain of Max which inhibits homodimer but not heterodimer DNA binding activity. 3. We will develop assays to determine the function of the N-terminal portion of the c-Myc protein, which is hypothesized to function in the enhancement of transcription. Conserved domains of Myc will be used to screen expression libraries and for affinity column, both of which will be used to isolate and then characterize the cellular factors that mediate Myc function. 4. We will continue our studies of myc-regulated cellular promoters to identify the key cellular targets through which myc transforms cells.
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