Evidence map›Paper›PMID 11521201›Full record

ArticleOncogene2001

The C-terminus of mutant p53 is necessary for its ability to interfere with growth arrest or apoptosis.

A Sigal, D Matas, N Almog, N Goldfinger, V Rotter

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–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

12 citing papers in PubMed.

  1. Reactivation ofInternational journal of molecular sciences · 2026
    Article
  2. Article
  3. p53 signaling in cancer progression and therapy.Cancer cell international · 2021
    Review
  4. Review
  5. Article
  6. p53 mutations in cancer.Nature cell biology · 2013
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

A SigalDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, 76100, Israel.
D Matas
N Almog
N Goldfinger
V Rotter

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ability to suppress wild type p53-independent apoptosis may play an important role in the oncogenicity of p53 mutant proteins. However, structural elements necessary for this activity are unknown. Furthermore, it is unclear whether this mutant p53 mediated inhibition is specific to the apoptotic pathway or a more general suppression of the cellular response to stress. We observed that an unmodified C-terminus was required for the suppression of apoptosis by the p53 135(Ala to Val) oncogenic p53 mutant. It was also required for the novel activity of G2 arrest suppression, the predominant response at low levels of genotoxic stress. These observations are consistent with a model whereby mutant p53 suppressive activity is not specific to the apoptotic pathway, but rather increases the threshold of genotoxic stress needed for a DNA damage response to occur. Furthermore, these observations indicate that it may be possible to selectively kill mutant p53 expressing cells based on the lower sensitivity of their growth arrest response.

Indexed as

ApoptosisMutationAnimalsCell DivisionCisplatinDNA DamageEtoposideG2 PhaseHumansMiceTumor Suppressor Protein p53CisplatinEtoposideTumor Suppressor Protein p53

Identifiers

PMID11521201

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.