Cold Spring Harbor Laboratory, Cold Spring
Harbor, New York 11724, USA.
lowe@cshl.org
Whereas p73 is closely related to the tumour-suppressor protein
p53, its contribution to tumour suppression and the spatial and temporal regulation
of its isoforms is unclear. It has now been established that p73 is a transcriptional
target of E2F1. Its ability to induce apoptosis in TP53-/-
cells indicates a tumour-control mechanism that runs parallel
to but independent of that mediated by p53. The new results illustrate a complex
cross-talk between p53, E2F1 and p73.
