The protein p53 is the most frequently mutated tumour suppressor to be
identified so far in human cancers(1,2). The ability of p53 to inhibi
t cell growth is due, at least in part, to its ability to bind to spec
ific DNA sequences and activate the transcription of target genes such
as that encoding the cell-cycle inhibitor p21(Waf1/Cip1) (ref. 3), A
gene has recently been identified that is predicted to encode a protei
n with significant amino-acid sequence similarity to p53 (ref, 4), In
particular, each of the p53 amino-acid residues implicated in direct s
equence-specific DNA binding is conserved in this protein(5). This gen
e, called p73, maps to the short arm of chromosome 1, and is found in
a region that is frequently deleted in neuroblastomas(6). Here we show
that p73 can, at least when overproduced, activate the transcription
of p53-responsive genes and inhibit cell growth in a p53-like manner b
y inducing apoptosis (programmed cell death).