Cited by 118Cancer-related Molecular PathwaysCell death mechanisms and regulationHeat shock proteins research

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Perp Is a Mediator of p53-Dependent Apoptosis in Diverse Cell Types

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Ihrie, Rebecca A., Reczek, Elizabeth, Horner, Jennifer S., Khachatrian, Leili, Sage, Julien, Jacks, Tyler, Attardi, Laura D.·2003·Current Biology

DOI 10.1016/j.cub.2003.10.055

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Abstract

The induction of apoptosis by the p53 protein is critical for its activity as a tumor suppressor. Although it is clear that p53 induces apoptosis at least in part by direct transcriptional activation of target genes, the set of p53 target genes that mediate p53 function in apoptosis in vivo remains to be well defined. The Perp (p53 apoptosis effector related to PMP-22) gene is highly expressed in cells undergoing p53-dependent apoptosis as compared to cells undergoing p53-dependent G1 arrest. Perp is a direct p53 target, and its overexpression is sufficient to induce cell death in fibroblasts, implicating it as an important component of p53 apoptotic function. Here, through the generation of Perp-deficient mice, we analyze the role of Perp in the p53 apoptosis pathway in multiple primary cell types by comparing the cell death responses of Perp null cells to those of wild-type and p53 null cells. These experiments demonstrate the involvement of Perp in p53-mediated cell death in thymocytes and neurons but not in E1A-expressing MEFs, indicating a cell type-specific role for Perp in the p53 cell death pathway. In addition, we show that Perp is not required for proliferation-associated functions of p53. Thus, Perp selectively mediates the p53 apoptotic response, and the requirement for Perp is dictated by cellular context.

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Authors: Ihrie, R. A., Reczek, E., Horner, J. S., Khachatrian, L., Sage, J., Jacks, T., & Attardi, L. D.
Affiliations: Stanford Medicine (US)
Massachusetts Institute of Technology (US)
Howard Hughes Medical Institute (US)
Corresponding author: Attardi, Laura D.
ORCID: Ihrie, Rebecca A.
Sage, Julien
Jacks, Tyler
Attardi, Laura D.
Venue: Current Biology
Publisher: Elsevier BV
Published: 2003-11
Volume: 13
Issue: 22
Pages: 1985-1990
ISSN: 0960-9822 (ISSN-L)
DOI: 10.1016/j.cub.2003.10.055
OpenAlex: W2095424453
Cited by: 118
References: 18
Citations by year: 2026: 1 · 2025: 4 · 2024: 2 · 2022: 9 · 2021: 2 · 2020: 4 · 2019: 4 · 2018: 4 · 2017: 6 · 2016: 3 · 2015: 5 · 2014: 2 · 2013: 5 · 2012: 7
FWCI: 3.90
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 3546 d)
doi.org/10.15223/policy-017 (stm-asf)
doi.org/10.15223/policy-037 (stm-asf)
doi.org/10.15223/policy-012 (stm-asf)
doi.org/10.15223/policy-029 (stm-asf)
doi.org/10.15223/policy-004 (stm-asf)
Locations: Current Biology (publishedVersion)
PubMed (publishedVersion)
Funders: National Cancer Institute (CA09302, R01CA093665, CA93665-01, T32CA009302)
Topics: Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
Keywords: PERP, p53, apoptosis, p53 target genes, tumor suppressor, thymocytes, neurons, G1 cell cycle arrest
MeSH terms: Animals, Membrane Proteins, Mice, Mutant Strains, Blotting, Southern, Blotting, Northern, Tumor Suppressor Protein p53, Apoptosis, In Situ Nick-End Labeling, Gene Expression Profiling, Mice

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Perp Is a Mediator of p53-Dependent Apoptosis in Diverse Cell Types

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