Execution of the cell-death programme requires the activation of a fam
ily of cysteine proteases known as caspases. Specific cellular protein
s are cleaved by caspases during apoptosis, including the retinoblasto
ma tumour-suppressor protein (RB1). A caspase-resistant RB1 can attenu
ate the death response to tumour necrosis factor alpha. The cleavage o
f RB1 during cell death, together with the increased cell death during
embryonic development of Rb-knockout mice, suggests that RB1 degradat
ion contributes to the activation of the cell-death pathway.