37AA – p53-derived apoptotic Peptide

…inducing apoptosis through non-transcriptional cytoplasmic processes. Ubiquitin ligase MDM2 ensures p53 remains inactive in unstressed cells inhibiting p53 transcriptional activity and promoting its degradation via ubiquitination. Modulation of p53 occurs…

Contributors

Inventor Institute
Kevin Ryan Cancer Research UK, Glasgow: The Beatson Institute
Cat. #: 152986
Research Fields: Apoptosis and autophagy;Cancer
Alternate name: pp
Product description: The transcription factor p53 reacts to diverse cellular stresses regulating target genes that induce senescence, apoptosis, DNA repair, cell cycle arrest or changes in metabolism. p53 is also capable of inducing apoptosis through non-transcriptional cytoplasmic processes. Ubiquitin ligase MDM2 ensures p53 remains inactive in unstressed cells inhibiting p53 transcriptional activity and promoting its degradation via ubiquitination. Modulation of p53 occurs through a variety of post-translational modifications, like phosphorylation and acetylation. The loss of p53 activity is routinely lost in human cancer. This is either due to mutation of the p53 gene or through a loss of cell signalling either, upstream or downstream of p53. The p53-derived peptide: 37AA induces cell death without the need to directly activate p53 target genes. The 37AA peptide also induces cell death in multiple tumour cell types but not in normal cells. 37AA binds directly to iASPP, disrupting the interaction between iASPP and p73 causing derepression of endogenous p73. This subsequently causes activation of p73 target genes and cell death. The peptide also functions in vivo, as administration of a transgene expressing this peptide resulted in tumour regression in a manner dependent on p73.
Additional notes: Transformation-related protein 53; TRP53
References:

Bell et al. 2007. J Clin Invest. 117(4):1008-18. PMID: 17347683.

A p53-derived apoptotic peptide derepresses p73 to cause tumor regression in vivo.

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