Evidence map›Paper›PMID 23690620›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Ninjurin1, a target of p53, regulates p53 expression and p53-dependent cell survival, senescence, and radiation-induced mortality.

Seong-Jun Cho, Andrea Rossi, Yong-Sam Jung, Wensheng Yan, Gang Liu, Jin Zhang, Min Zhang, Xinbin Chen

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing 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

37 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Review
  3. The role of NINJ1 in diseases.Cell death discovery · 2026
    Review
  4. Review
  5. Review
  6. NINJ1 impairs the anti-inflammatory function of hUC-MSCs with synergistic IFN-γ and TNF-α stimulation.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2025
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Observational
  13. Article
  14. Article
  15. Article
  16. Role of p53 in Regulating Radiation Responses.Life (Basel, Switzerland) · 2022
    Review
  17. Article
  18. Article
  19. Article
  20. 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

8 authors at 1 institution in 1 country.

Seong-Jun ChoComparative Oncology Laboratory, University of California, Davis, CA 95616, USA.
Andrea Rossi
Yong-Sam Jung
Wensheng Yan
Gang Liu
Jin Zhang
Min Zhang
Xinbin Chen
University of California, Davis · US

Funding

Staff InvestigatorsP30CA093373 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI Laura Marcu · 2002 to 2026
$84.9M
Mechanism of p53-Mediated Tumor SuppressionR01CA076069 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, XINBIN · 2002 to 2017
$4.5M
The transcriptional activity of p63, a p53 family memberR01CA102188 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN, XINBIN · 2003 to 2012
$2.9M
NCI NIH HHS CA076068NCI NIH HHS CA102188NCI NIH HHS P30 CA093373NCI NIH HHS R01 CA076069NCI NIH HHS R01 CA102188
6 · The paper itself

Abstract

The tumor suppressor protein p53 plays a crucial role in coordinating cellular processes, such as cell cycle arrest, apoptosis, and senescence. The nerve injury-induced protein 1 (Ninjurin1, Ninj1) is a homophilic adhesion molecule and involved in nerve regeneration. Interestingly, Ninj1 is found to be overexpressed in human cancer, but its role in tumorigenesis is not clear. Here, we found that Ninj1 is transcriptionally regulated by p53 and can be induced by DNA damage in a p53-dependent manner. We also found that knockout or knockdown of Ninj1 increases p53 expression potentially through enhanced p53 mRNA translation. In addition, we found that Ninj1 deficiency suppresses cell proliferation but enhances apoptosis and premature senescence in a p53-dependent manner. Consistent with this, we found that mice heterozygous in ninj1 are hypersensitive to ionizing radiation-induced lethality, along with increased expression of p53 in thymus. Taken together, we provided evidence that Ninj1 is a p53 target and modulates p53 mRNA translation and p53-dependent premature senescence, cell proliferation, apoptosis, and radiation-induced mortality in vitro and in vivo. Thus, we postulate that as a membrane adhesion molecule, Ninj1 is an ideal target to regulate p53 activity via the p53-Ninj1 loop.

Indexed as

AnimalsBlotting, NorthernBlotting, WesternCell Adhesion Molecules, NeuronalCell SurvivalCellular SenescenceChromatin ImmunoprecipitationColony-Forming Units AssayDNA PrimersFluorescent Antibody TechniqueGamma RaysGene Expression RegulationLuciferasesMiceMice, KnockoutNerve Growth FactorsCell Adhesion Molecules, NeuronalDNA PrimersLuciferasesNerve Growth FactorsNinj1 protein, mouseSulfur RadioisotopesTumor Suppressor Protein p53cellular senescenceradiosensitivity

Identifiers

PMID23690620
PMCPMC3677487
OpenAlexW2058337912

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.