Evidence map›Paper›PMID 22804246›Full record

ArticleCurrent molecular medicine2012

p53 is an important regulator of CCL2 gene expression.

X Tang, M Asano, A O'Reilly, A Farquhar, Y Yang, S Amar

Abstract read
In one paragraph

Article in Current molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed, 29 citations in OpenAlex.

  1. Frontiers in immunology · 2026
    Article
  2. Article
  3. Review
  4. Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2022
    Article
  5. Article
  6. P53 in the impaired lungs.DNA repair · 2020
    Review
  7. Deficiency of miR-208a Exacerbates CClHepatology communications · 2020
    Article
  8. Article
  9. Article
  10. The Photomodulation Activity of Metformin Against Oral Microbiome.Journal of lasers in medical sciences · 2019
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. p53 suppresses CCL2-induced subcutaneous tumor xenograft.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  17. Article
  18. Article
  19. Oral bacteria and cancer.PLoS pathogens · 2014
    Review
  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

6 authors at 1 institution in 1 country.

X TangCenter for Anti- Inflammatory Therapeutics, Boston University, 650 Albany Street, X- 343, Boston, MA 02118, USA. xrtang@bu.edu
M Asano
A O'Reilly
A Farquhar
Y Yang
S Amar
Boston University · US

Funding

Role of LITAF in Inflammatory ProcessesR01DE014079 · NIDCR · NEW YORK MEDICAL COLLEGE · PI AMAR, SALOMON · 2002 to 2016
$5.4M
NIDCR NIH HHS R01 DE014079NIDCR NIH HHS R01DE014079
6 · The paper itself

Abstract

The p53 protein is a sequence-specific DNA-binding factor that regulates inflammatory genes such as CCL2/MCP-1 that may play a role in various diseases. A recent study has indicated that the knockdown of human p53 leads to a strong negative regulation of CCL2 induction. We are therefore interested in how p53 regulates CCL2 gene expression. In the following study, our findings indicate that UV-induced p53 accumulation in mouse macrophages significantly decreases LPS-induced CCL2 production, and that p53 binds to CCL2 5'UTR in the region (16-35). We also found that a p53 domain (p53pep170) mimics full length p53 to down-regulate CCL2 promoter activity. Treatment of p53-deficient mouse primary macrophages with synthetic p53pep170 was found to decrease LPS-induced production of CCL2 without association with cellular endogenous p53. CCL2 production induced by lentiCLG in human monocytes or mouse primary macrophages was blocked in the presence of p53pep170. Overall, these results demonstrate that p53 or its derived peptide (p53pep170) is an important regulator of CCL2 gene expression via its binding activity, and acts as a novel model for future studies linking p53 and its short peptide to pave the way to possible pharmaceutical intervention of CCL2-mediated inflammatory and cancer diseases.

Indexed as

5' Untranslated RegionsAnimalsBase SequenceBinding SitesCell Line, TumorChemokine CCL2Gene Expression RegulationGenes, ReporterHumansInflammation MediatorsInterleukin-1betaLipopolysaccharidesLuciferasesMacrophagesMiceMice, Knockout5' Untranslated RegionsCcl2 protein, mouseChemokine CCL2Inflammation MediatorsInterleukin-1betaLipopolysaccharidesLuciferasesPeptide FragmentsTumor Suppressor Protein p53

Identifiers

PMID22804246
PMCPMC3786129
OpenAlexW2078374333

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.