Interaction of c-Myc with the pRb-related protein p107 results in inhibition of c-Myc-mediated transactivation.

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Abstract
The product of the c‐myc proto‐oncogene, c‐Myc, is a sequence‐specific DNA binding protein with an N‐terminal transactivation domain and a C‐terminal DNA binding domain. Several lines of evidence indicate that c‐Myc activity is essential for normal cell cycle progression. Since the abundance of c‐Myc during the cell cycle is constant, c‐Myc's activity may be regulated at a post‐translational level. We have shown previously that the N‐terminus of c‐Myc can form a specific complex with the product of the retinoblastoma gene, pRb, in vitro. These data suggested a model in which pRb, or pRb‐related proteins, regulate c‐Myc activity through direct binding. We show here that the pRb‐related protein p107, but not pRb itself, forms a specific complex with the N‐terminal transactivation domain of c‐Myc in vivo. Binding of p107 to c‐Myc causes a significant inhibition of c‐Myc transactivation. Expression of c‐Myc releases cells from a p107‐induced growth arrest, but not from pRb‐induced growth arrest. Our data suggest that p107 can control c‐Myc activity through direct binding to the transactivation domain and that c‐Myc is a target for p107‐mediated growth suppression.

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