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The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

PERP, an apoptosis-associated target of p53, is a novel member of the PMP-22/gas3 family

Open access
Attardi, Laura D., Reczek, Elizabeth E., Cosmas, Corinna, Demicco, Elizabeth G., McCurrach, Mila E., Lowe, Scott W., Jacks, Tyler·2000·Genes & Development

Abstract

The p53 tumor suppressor activates either cell cycle arrest or apoptosis in response to cellular stress. Mouse embryo fibroblasts (MEFs) provide a powerful primary cell system to study both p53-dependent pathways. Specifically, in response to DNA damage, MEFs undergo p53-dependent G 1 arrest, whereas MEFs expressing the adenovirus E1A oncoprotein undergo p53-dependent apoptosis. As the p53-dependent apoptosis pathway is not well understood, we sought to identify apoptosis-specific p53 target genes using a subtractive cloning strategy. Here, we describe the characterization of a gene identified in this screen, PERP, which is expressed in a p53-dependent manner and at high levels in apoptotic cells compared with G 1-arrested cells. PERP induction is linked to p53-dependent apoptosis, including in response to E2F-1-driven hyperproliferation. Furthermore, analysis of the PERP promoter suggests that PERP is directly activated by p53. PERP shows sequence similarity to the PMP-22/gas3 tetraspan membrane protein implicated in hereditary human neuropathies such as Charcot–Marie–Tooth. Like PMP-22/gas3, PERP is a plasma membrane protein, and importantly, its expression causes cell death in fibroblasts. Taken together, these data suggest that PERP is a novel effector of p53-dependent apoptosis.

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Crossref · 10.1101/gad.14.6.704

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Metadata

Authors
Attardi, L. D., Reczek, E. E., Cosmas, C., Demicco, E. G., McCurrach, M. E., Lowe, S. W., & Jacks, T.
Venue
Genes & Development
Published
2000-03-15
Volume
14
Issue
6
Pages
704-718
ISSN
  • 0890-9369 (ISSN-L)
  • 1549-5477
OpenAlex
W2155363874
Cited by
397
References
9
Type
posted content
Language
en
Open access
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