Evidence map›Paper›PMID 10733530›Full record

ArticleGenes & development2000

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

L D Attardi, E E Reczek, C Cosmas, E G Demicco, M E McCurrach, S W Lowe, T Jacks

Erratum issuedOpen access · diamondAbstract read
In one paragraph

Article in Genes & development, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 167 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
167citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

167 citing papers in PubMed, 1 synthesis or guideline pooled it, 397 citations in OpenAlex.

  1. A systematic review of p53 regulation of oxidative stress in skeletal muscle.Redox report : communications in free radical research · 2018
    Pooled it
  2. Trial
  3. Article
  4. Review
  5. PERP suppresses breast cancer metastasis via the ATF3-HSPA6 signaling pathway.The Journal of international medical research · 2025
    Article
  6. Article
  7. Article
  8. Article
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  11. Article
  12. Review
  13. Article
  14. DecipheringmSystems · 2024
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

107 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

7 authors at 4 institutions in 1 country.

L D AttardiDepartment of Biology and Center for Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139 USA.
E E Reczek
C Cosmas
E G Demicco
M E McCurrach
S W Lowe
T Jacks
Cold Spring Harbor Laboratory · USMassachusetts Institute of Technology · USCenter for Cancer Research · USHoward Hughes Medical Institute · US

Funding

VIRAL TRANSACTIVATIONP01CA013106 · NCI · COLD SPRING HARBOR LABORATORY · PI William Richard McCombie · 1985 to 2026
$116.8M
NCI NIH HHS CA13106NCI NIH HHS P01 CA013106
6 · The paper itself

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.

Indexed as

Carrier ProteinsCell Cycle ProteinsDNA-Binding ProteinsAmino Acid SequenceAnimalsApoptosisBase SequenceCell LineDNA, ComplementaryE2F1 Transcription FactorE2F Transcription FactorsGene Expression RegulationHumansMembrane ProteinsMiceMolecular Sequence DataArid4a protein, mouseCarrier ProteinsCell Cycle ProteinsDNA-Binding ProteinsDNA, ComplementaryE2F1 protein, humanE2f1 protein, mouseE2F1 Transcription FactorE2F Transcription FactorsMembrane ProteinsMyelin ProteinsPerp protein, mousePMP22 protein, humanPmp22 protein, mouseRetinoblastoma-Binding Protein 1Transcription Factor DP1Transcription FactorsTumor Suppressor Protein p53

Identifiers

PMID10733530
PMCPMC316461
OpenAlexW2155363874

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.