Evidence map›Paper›PMID 21245379›Full record

ArticleMolecular and cellular biology2011

The codon 72 polymorphism of p53 regulates interaction with NF-{kappa}B and transactivation of genes involved in immunity and inflammation.

Amanda K Frank, Julia I-Ju Leu, Yan Zhou, Karthik Devarajan, Tatiana Nedelko, Andres Klein-Szanto, Monica Hollstein, Maureen E Murphy

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

77 citing papers in PubMed, 112 citations in OpenAlex.

  1. Article
  2. Article
  3. Observational
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Breast care (Basel, Switzerland) · 2024
    Article
  10. A Missense Variant inInternational journal of molecular sciences · 2024
    Article
  11. Article
  12. Article
  13. p53 and Myofibroblast Apoptosis in Organ Fibrosis.International journal of molecular sciences · 2023
    Review
  14. Review
  15. Targeting PSAT1 to mitigate metastasis in tumors with p53-72Pro variant.Signal transduction and targeted therapy · 2023
    Article
  16. Article
  17. Role of p53 in Regulating Radiation Responses.Life (Basel, Switzerland) · 2022
    Review
  18. TP53 Codon 72 Polymorphism and the Risk of Colorectal Cancer in an Azerbaijani Population.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2022
    Article
  19. Review
  20. Review

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

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

8 authors at 4 institutions in 3 countries.

Amanda K FrankFox Chase Cancer Center, W209, 333 Cottman Avenue, Philadelphia, PA 19111, USA.
Julia I-Ju Leu
Yan Zhou
Karthik Devarajan
Tatiana Nedelko
Andres Klein-Szanto
Monica Hollstein
Maureen E Murphy
Fox Chase Cancer Center · USGerman Cancer Research Center · DEUniversity of Leeds · GBUniversity of Pennsylvania · US

Funding

Functional Analysis of p53 Polymorphic Variants - Diversity SupplementR01CA102184 · NCI · WISTAR INSTITUTE · PI Maureen E. Murphy · 2005 to 2026
$7.4M
NCI NIH HHS R01 CA102184
6 · The paper itself

Abstract

A common polymorphism at codon 72 in the p53 tumor suppressor gene encodes either proline (P72) or arginine (R72). Several groups have reported that in cultured cells, this polymorphism influences p53's transcriptional, senescence, and apoptotic functions. However, the impact of this polymorphism within the context of a living organism is poorly understood. We generated knock-in mice with the P72 and R72 variants and analyzed the tissues of these mice for apoptosis and transcription. In the thymus, we find that the P72 variant induces increased apoptosis following ionizing radiation, along with increased transactivation of a subset of p53 target genes, which includes murine Caspase 4 (also called Caspase 11), which we show is a direct p53 target gene. Interestingly, the majority of genes in this subset have roles in inflammation, and their promoters contain NF-κB binding sites. We show that caspase 4/11 requires both p53 and NF-κB for full induction after DNA damage and that the P72 variant shows increased interaction with p65 RelA, a subunit of NF-κB. Consistent with this, we show that P72 mice have a markedly enhanced response to inflammatory challenge compared to that of R72 mice. Our data indicate that the codon 72 polymorphism impacts p53's role in inflammation.

Indexed as

Polymorphism, GeneticTranscriptional ActivationAnimalsApoptosisCaspasesCaspases, InitiatorCells, CulturedFibroblastsGene Knock-In TechniquesImmunityInflammationMiceMice, Inbred C57BLNF-kappa Bras ProteinsThymus GlandCasp4 protein, mouseCaspasesCaspases, InitiatorNF-kappa Bras ProteinsTranscription Factor RelATumor Suppressor Protein p53

Identifiers

PMID21245379
PMCPMC3067895
OpenAlexW2097334501

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.