Evidence map›Paper›PMID 20052674›Full record

ArticleJournal of cellular biochemistry2010

TAp63 is a transcriptional target of NF-kappaB.

Junfeng Wu, Johann Bergholz, Jinin Lu, Gail E Sonenshein, Zhi-Xiong Jim Xiao

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. p63-related signaling at a glance.Journal of cell science · 2020
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Role of p63 in Development, Tumorigenesis and Cancer Progression.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2012
    Article
  13. 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

5 authors at 1 institution in 1 country.

Junfeng WuDepartment of Biochemistry, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
Johann Bergholz
Jinin Lu
Gail E Sonenshein
Zhi-Xiong Jim Xiao
Boston University · US

Funding

Role of MDM2 in Cell Proliferation and TumorigenesisR01CA079804 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI XIAO, ZHI-XIONG JIM · 1999 to 2010
$2.2M
Roles of NF-kB/Rel in the pathogenesis of breast cancerR01CA129129 · NCI · TUFTS UNIVERSITY BOSTON · PI SONENSHEIN, GAIL E. · 2008 to 2012
$1.7M
Regulation of p53 in response to genotoxic stressR01GM070017 · NIGMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI XIAO, ZHI-XIONG JIM · 2003 to 2006
$1.2M
NCI NIH HHS CA129129NCI NIH HHS CA79804NCI NIH HHS R01 CA079804NCI NIH HHS R01 CA129129NIGMS NIH HHS GM70017NIGMS NIH HHS R01 GM070017
6 · The paper itself

Abstract

The p53 homologue p63 encodes multiple protein isoforms either with (TA) or without (DeltaN) the N-terminal transactivation domain. Accumulating evidence indicates that TAp63 plays an important role in various biological processes, including cell proliferation, differentiation, and apoptosis. However, how TAp63 is regulated remains largely unclear. In this study, we demonstrate that NF-kappaB induces TAp63 gene expression. The responsible elements for NF-kappaB-mediated TAp63 induction are located within the region from -784 to -296 bp in the TAp63 promoter, which contains two NF-kappaB binding sites. Ectopic expression of RelA stimulates TAp63 promoter-driven reporter activity and increases endogenous TAp63 mRNA levels. Inhibition of NF-kappaB by IkappaBalpha super-repressor or with a chemical inhibitor leads to down regulation of TAp63 mRNA expression and activity. In addition, mutations in the critical NF-kappaB-binding sites significantly abolish the effects of NF-kappaB on TAp63. Activation of NF-kappaB by TNFalpha enhances p50/RelA binding to the NF-kappaB binding sites. Furthermore, we show that an Sp1 site adjacent to the NF-kappaB sites plays a role in NF-kappaB-mediated upregulation of TAp63. Taken together, these data reveal that TAp63 is a transcriptional target of NF-kappaB, which may play a role in cell proliferation, differentiation and survival upon NF-kappaB activation by various stimuli.

Indexed as

Transcriptional ActivationBinding SitesCell LineHumansNF-kappa BPromoter Regions, GeneticRNA, MessengerSp1 Transcription FactorTrans-ActivatorsTranscription Factor RelATranscription FactorsTumor Suppressor ProteinsUp-RegulationNF-kappa BRNA, MessengerSp1 Transcription FactorTP63 protein, humanTrans-ActivatorsTranscription Factor RelATranscription FactorsTumor Suppressor Proteins

Identifiers

PMID20052674
PMCPMC2873845
OpenAlexW2120489240

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.