Evidence map›Paper›PMID 20506119›Full record

ArticleJournal of cellular biochemistry2010

EGR1, EGR2, and EGR3 activate the expression of their coregulator NAB2 establishing a negative feedback loop in cells of neuroectodermal and epithelial origin.

Joerg Kumbrink, Kathrin H Kirsch, Judith P Johnson

Abstract 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 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
2.6field-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

51 citing papers in PubMed, 82 citations in OpenAlex.

  1. EGR3 Promotes Glioblastoma Cell Growth with Upregulation of MYC and CDK1.International journal of molecular sciences · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Epigenetic landscape revealsFrontiers in nutrition · 2025
    Article
  6. Review
  7. Pannexin 1 crosstalk with the Hippo pathway in malignant melanoma.bioRxiv : the preprint server for biology · 2024
    Article
  8. Article
  9. Nur77 Mediates Anaphylaxis by Regulating miR-21a.Current issues in molecular biology · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Inducible CRISPR Epigenome Systems Mimic Cocaine Induced Bidirectional Regulation of Nab2 and Egr3.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

3 authors at 2 institutions in 2 countries.

Joerg KumbrinkInstitute for Immunology, University of Munich, Munich 80336, Germany.
Kathrin H Kirsch
Judith P Johnson
Boston University · USLudwig-Maximilians-Universität München · DE

Funding

Functional role of p130Cas/BCAR1 in breast cancerR01CA106468 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI KIRSCH, KATHRIN H · 2005 to 2009
$1.4M
NCI NIH HHS CA106468NCI NIH HHS R01 CA106468
6 · The paper itself

Abstract

The inducible zinc finger transcription factors EGR1, EGR2, and EGR3 regulate the expression of numerous genes involved in differentiation, growth, and response to extracellular signals. Their activity is modulated in part through NAB2 which is induced by the same stimuli. In melanoma and carcinoma cells EGR1 activates NAB2 expression. In T lymphocytes EGR2 and EGR3 have been shown to inhibit NAB2 expression. Therefore, we investigated the influence of EGR2 and EGR3 on NAB2 expression in melanoma and carcinoma cells. Here, we show that like EGR1, EGR2 and EGR3 induced NAB2 expression in these cells. EGR1 and EGR3 act in concert on the NAB2 promoter and are more potent activators of NAB2 transcription than EGR2. EGR1-, EGR2-, and EGR3-induced NAB2 promoter activity is mediated through similar cis-regulatory elements and the activation by each EGR is repressed by NAB2. Kinetic studies suggest that induction of EGR1 leads to low NAB2 expression, while EGR2 and EGR3 are necessary for maximal and sustained expression. As already shown for EGR1, reduction of EGR2 or EGR3 expression by siRNAs reduced endogenous NAB2 levels. Depletion of EGR3 also resulted in a reduction of EGR2 levels confirming EGR2 as a target gene of EGR3. Our results suggest that in many cells of neuroectodermal and epithelial origin EGR1, EGR2, and EGR3 activate NAB2 transcription which is in turn repressed by NAB2, thus establishing a negative feedback loop. This points to a complex relationship between the EGR factors and NAB2 expression likely depending on the cellular context.

Indexed as

AnimalsCell Line, TumorEarly Growth Response Protein 1Early Growth Response Protein 2Early Growth Response Protein 3Epithelial CellsFeedback, PhysiologicalGene Expression RegulationHumansNeural PlatePromoter Regions, GeneticRepressor ProteinsRNA, Small InterferingT-LymphocytesTranscription, GeneticEarly Growth Response Protein 1Early Growth Response Protein 2Early Growth Response Protein 3EGR1 protein, humanEGR2 protein, humanEGR3 protein, humanNAB2 protein, humanRepressor ProteinsRNA, Small Interfering

Identifiers

PMID20506119
PMCPMC2930072
OpenAlexW2099141996

What OpenQuestion holds

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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.