Transcription-independent p53 apoptosis: an alternative route to death.
Apoptosis induced by p53 is firmly established as a central mechanism of tumour suppression. In addition to its complex functions as a nuclear transcription factor, p53 can act in the cytosol and mitochondria to promote apoptosis through transcription-independent mechanisms. Recent studies have shown that physical and functional interactions of p53 with various members of the Bcl-2 family provide the basis for this alternative route of p53-mediated cell death. However, different models of how these interactions promote apoptosis have been proposed. This review focuses on the mechanisms, regulation and physiological roles of transcription-independent p53 activities and highlights recent findings suggesting that the utilisation of these activities provides a promising alternative strategy for p53-based cancer therapy.
Speidel
Daniel
D
Cell Transformation Unit, Children's Medical Research Institute, 214 Hawkesbury Road, Westmead 2145 NSW, Australia. dspeidel@cmri.org.au
D000818:Animals; D017209:Apoptosis; D006801:Humans; D009369:Neoplasms / Q000235:genetics / Q000378:metabolism / Q000628:therapy; D015398:Signal Transduction; D014158:Transcription, Genetic; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism*
D016159:Tumor Suppressor Protein p53