The tumor suppressor p53 exerts its antioncogenic effects in cells chiefly
by regulating their progression through the cell cycle and by inducing cell
death. It has been claimed that p53-transduced apoptosis involves the deat
h receptor CD95 (Fas/APO-1). We report that thymocytes from mice Lacking fu
nctional Fas ligand (gld) show normal sensitivity to apoptosis transduced b
y p53, and that hepatocytes from p53(-/-) mice have normal sensitivity to a
poptosis triggered through ligation of CD95, p53 and CD95, therefore, funct
ion in independent pathways to cell death in these diverse fell types.