Evidence map›Paper›PMID 23230510›Full record

ArticleScientific reports2012

Two distinct knockout approaches highlight a critical role for p53 in rat development.

Masaki Kawamata, Takahiro Ochiya

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 36% of its field
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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. p53 Mutant p53International journal of biological sciences · 2019
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
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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

2 authors at 1 institution in 1 country.

Masaki KawamataDivision of Molecular and Cellular Medicine, National Cancer Center Research Institute , 1-1, Tsukiji, 5-chome, Chuo-ku, Tokyo 104-0045, Japan.
Takahiro Ochiya
National Cancer Research Institute · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gene targeting in embryonic stem cells (ESCs) has become the principal technology for generating knockout models. Although numerous studies have predicted that the disruption of p53 leads to increased developmental anomalies and malignancies, most p53 knockout mice develop normally. Therefore, the role of p53 in animal development was examined using rat knockout models. Conventionally generated homozygous KO males developed normally, whereas females rarely survived due to neural tube defects. Mutant chimeras generated via blastocyst injection with p53-null ESCs exhibited high rates of embryonic lethality in both sexes. This phenotype could be observed in one month by the use of zinc-finger nucleases. The p53-null ESCs were resistant to apoptosis and differentiation, and exhibited severe chromosome instabilities in the chimera-contributed cells, suggesting an essential role for p53 in maintaining ESC quality and genomic integrity. These results demonstrate that p53 functions as a guardian of embryogenesis in the rats.

Indexed as

AnimalsApoptosisBlastocystCell DifferentiationCell LineChromosomal InstabilityEmbryonic DevelopmentEmbryonic Stem CellsFemaleGene Expression ProfilingGene Knockout TechniquesHomozygoteMaleModels, AnimalRatsTumor Suppressor Protein p53Tumor Suppressor Protein p53

Identifiers

PMID23230510
PMCPMC3517977
OpenAlexW1966961951

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.