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c-Myb Regulates Cell Identity

    Different truncations of the c-Myb protein (dCd, dCC, CCd) or v-Myb (dVd), which also contains a number of amino acid substitutions relative to c-Myb, cause the proliferation of blood cells that are blocked at different specific stages of differentiation (1). Reversion of the amino acid substitutions in different domains of v-Myb can also influence the phenotype of the transformed cells (2,3). Overexpression of wild type c-Myb protein (CCC) causes the proliferation of immature precursors which can still undergo spontaneous differentiation (4). These results suggest that the wild type protein can adopt different conformations, resulting in the sequential regulation of different stage-specific genes. In contrast, the truncated proteins may be stuck in a single conformation resulting in the regulation of only one stage-specific set of genes.

1. Grasser, Graf, and Lipsick, Molec Cell Biol 11: 3987-3996 (1990).

2. Introna, Golay, Frampton, Nakano, Ness and Graf, Cell 63: 1289-1297 (1990).

3. Dini, Eltman and Lipsick, J Virol 69: 2515-2524 (1995).

4. Fu and Lipsick, Cell Growth Diff 8:35-45 (1997).