Evidence map›Paper›PMID 21454683›Full record

ArticleThe Journal of biological chemistry2011

Cancer susceptibility polymorphism of p53 at codon 72 affects phosphorylation and degradation of p53 protein.

Chikako Ozeki, Yuichiro Sawai, Tatsuhiro Shibata, Takashi Kohno, Koji Okamoto, Jun Yokota, Fumio Tashiro, Sei-ichi Tanuma, Ryuichi Sakai, Tatsuya Kawase and 3 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Identification of IDUA and WNT16 Phosphorylation-Related Non-Synonymous Polymorphisms for Bone Mineral Density in Meta-Analyses of Genome-Wide Association Studies.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2016
    Pooled it
  2. Review
  3. Alterations in p53 Influence hTERT, VEGF and MMPs Expression in Oral Cancer Patients.Asian Pacific journal of cancer prevention : APJCP · 2022
    Article
  4. Article
  5. Article
  6. PHLDA3 is a novel tumor suppressor of pancreatic neuroendocrine tumors.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  7. Article
  8. P53 codon 72 polymorphism in Taiwanese breast cancer patients.The Kaohsiung journal of medical sciences · 2013
    Article
  9. Article
  10. Article
  11. UBE4B: a promising regulatory molecule in neuronal death and survival.International journal of molecular sciences · 2012
    Review
  12. Review
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

13 authors at 6 institutions in 4 countries.

Chikako OzekiRadiobiology Division, National Cancer Center Research Institute, Tsukiji 5-1-1, Tokyo 104-0045, Japan.
Yuichiro Sawai
Tatsuhiro Shibata
Takashi Kohno
Koji Okamoto
Jun Yokota
Fumio Tashiro
Sei-ichi Tanuma
Ryuichi Sakai
Tatsuya Kawase
Issay Kitabayashi
Yoichi Taya
Rieko Ohki
Molecular Oncology (United States) · USNational Cancer Centre Japan · JPCancer Genomics Centre · NLGenesis Research Institute · JPNational University of Singapore · SGTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The common polymorphism of p53 at codon 72, either encoding proline or arginine, has drawn attention as a genetic factor associated with clinical outcome or cancer risk for the last 2 decades. We now show that these two polymorphic variants differ in protein structure, especially within the N-terminal region and, as a consequence, differ in post-translational modification at the N terminus. The arginine form (p53-72R) shows significantly enhanced phosphorylation at Ser-6 and Ser-20 compared with the proline form (p53-72P). We also show diminished Mdm2-mediated degradation of p53-72R compared with p53-72P, which is at least partly brought about by higher levels of phosphorylation at Ser-20 in p53-72R. Furthermore, enhanced p21 expression in p53-72R-expressing cells, which is dependent on phosphorylation at Ser-6, was demonstrated. Differential p21 expression between the variants was also observed upon activation of TGF-β signaling. Collectively, we demonstrate a novel molecular difference and simultaneously suggest a difference in the tumor-suppressing function of the variants.

Indexed as

CodonGenetic Predisposition to DiseaseNeoplasmsPolymorphism, GeneticProtein Processing, Post-TranslationalTumor Suppressor Protein p53Cell LineHumansPhosphorylationProto-Oncogene Proteins c-mdm2Signal TransductionTransforming Growth Factor betaCodonMDM2 protein, humanProto-Oncogene Proteins c-mdm2TP53 protein, humanTransforming Growth Factor betaTumor Suppressor Protein p53

Identifiers

PMID21454683
PMCPMC3093897
OpenAlexW2076613705

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.