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PERP (p53 apoptosis effector related to PMP22) is a tetraspan transmembrane protein and a direct transcriptional target of the tumor suppressor p53, primarily induced in response to apoptotic signals but not during cell cycle arrest[1][2][3]. Highly expressed at the plasma membrane, PERP regulates cell death downstream of p53 by promoting apoptosis; its induction precedes the onset of cell death and can suffice to cause apoptosis when overexpressed[1][2][3][5]. Functionally, PERP is a member of the peripheral myelin protein 22 (PMP22) family, sharing structural similarity with cell adhesion molecules, and is crucial for maintaining epithelial integrity and tissue-specific cell survival, particularly in stressed or damaged tissues[2][4]. PERP may also amplify p53 activity by modulating nuclear localization and the p53–MDM2 regulatory loop[3]. Its dysregulation or loss has been implicated in reduced cellular response to apoptotic stimuli and in cancer. No known drugs directly target PERP, but its molecular features make it a promising candidate for therapies aimed at p53-mediated apoptosis or cancer treatment[3][5].
Induction of apoptosis through p53 pathway activation Modulation of p53–MDM2 complex and enhancement of p53 transcriptional activity
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