Evidence map›Paper›PMID 20499882›Full record

ArticleBiochemistry2010

Nitration of the tumor suppressor protein p53 at tyrosine 327 promotes p53 oligomerization and activation.

Vasily A Yakovlev, Alexander S Bayden, Paul R Graves, Glen E Kellogg, Ross B Mikkelsen

Abstract read
In one paragraph

Article in Biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 54 citations in OpenAlex.

  1. Nitration in cancer signaling.Redox biology · 2026
    Review
  2. p53: The Multifaceted Roles of Covalent Modifications in Cancer.Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  3. Review
  4. Review
  5. Article
  6. Nitrative Stress and Auditory Dysfunction.Pharmaceuticals (Basel, Switzerland) · 2022
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Signaling and stress: The redox landscape in NOS2 biology.Free radical biology & medicine · 2015
    Review
  15. Article
  16. Review
  17. Stem cells, redox signaling, and stem cell aging.Antioxidants & redox signaling · 2014
    Review
  18. Review
  19. Article
  20. 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

5 authors at 1 institution.

Vasily A YakovlevDepartment of Radiation Oncology, Massey Cancer Center, Virginia Commonwealth University, Richmond, Virginia 23298, USA.
Alexander S Bayden
Paul R Graves
Glen E Kellogg
Ross B Mikkelsen
VCU Massey Comprehensive Cancer Center

Funding

RADIOSENSITIZATION OF MALIGNANT GLIOMAS BY VIRAL TRANSDUCTION WITH WILD-TYPE P53P01CA072955 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI VALERIE, KRISTOFFER CARL · 1998 to 2007
$6.0M
RAD-Induced Nitric Oxide &Cellular RadiosensitivityR01CA090881 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI MIKKELSEN, ROSS B · 2002 to 2012
$2.4M
New Hydropathy-Based computer Tools for Drug DiscoveryR01GM071894 · NIGMS · VIRGINIA COMMONWEALTH UNIVERSITY · PI KELLOGG, GLEN EUGENE · 2005 to 2009
$1.1M
Training in Radiation Oncology Translational ResearchT32CA113277 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI MIKKELSEN, ROSS B · 2007 to 2011
$997k
NCI NIH HHS P01 CA072955NCI NIH HHS R01 CA090881NCI NIH HHS R01CA90881NCI NIH HHS T32 CA113277NIGMS NIH HHS GM071894NIGMS NIH HHS R01 GM071894
6 · The paper itself

Abstract

Previous studies demonstrate that nitric oxide (NO) promotes p53 transcriptional activity by a classical DNA damage responsive mechanism involving activation of ATM/ATR and phosphorylation of p53. These studies intentionally used high doses of NO donors to achieve the maximum DNA damage. However, lower concentrations of NO donors also stimulate rapid and unequivocal nuclear retention of p53 but apparently do not require ATM/ATR-dependent p53 phosphorylation or total p53 protein accumulation. To identify possible mechanisms for p53 activation at low NO levels, the role of Tyr nitration in p53 activation was evaluated. Low concentrations of the NO donor, DETA NONOate (<200 microM), exclusively nitrate Tyr327 within the tetramerization domain promoting p53 oligomerization, nuclear accumulation, and increased DNA-binding activity without p53 Ser15 phosphorylation. Molecular modeling indicates that nitration of one Tyr327 stabilizes the dimer by about 2.67 kcal mol(-1). Significant quantitative and qualitative differences in the patterns of p53-target gene modulation by low (50 microM), non-DNA-damaging and high (500 microM), DNA-damaging NO donor concentrations were shown. These results demonstrate a new posttranslational mechanism for modulating p53 transcriptional activity responsive to low NO concentrations and independent of DNA damage signaling.

Indexed as

BiopolymersCell Line, TumorElectrophoretic Mobility Shift AssayHumansMass SpectrometryModels, MolecularNitratesNitric Oxide DonorsNitric Oxide SynthasePhosphorylationThermodynamicsTumor Suppressor Protein p53BiopolymersNitratesNitric Oxide DonorsNitric Oxide SynthaseTumor Suppressor Protein p53

Identifiers

PMID20499882
PMCPMC2892261
OpenAlexW2007651247

What OpenQuestion holds

Textmetadata
LicenceTDM
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.