CONFORMATIONAL CHANGE OF P53 PROTEIN IN GROWTH FACTOR-STIMULATED HUMAN MYELOGENOUS LEUKEMIA-CELLS

Frequent point mutations of the p53 tumor suppressor gene have been de tected in solid tumors but not in acute myelogenous leukemia (AML). Th e inactivation of the suppressor function of the p53 protein in AML ce lls may be achieved through the acquisition of a mutant-like conformat ion. We provide evidence in this report that the p53 protein in AML ce lls switches to a mutant-like conformation in response to growth facto r stimulation, and we propose that the conformation of p53 protein is one of the molecular mechanisms in determining whether the cells proli ferate or enter apoptosis. We also show that wild-type p53 with mutant -like conformation is not equivalent to mutant p53 in their stability, which is consistent with the fact they have very different biological activities in the cells.