Evidence map›Paper›PMID 19675674›Full record

ArticlePloS one2009

GSK3beta is involved in JNK2-mediated beta-catenin inhibition.

Dong Hu, Xiuli Bi, Wenfeng Fang, Anjia Han, Wancai Yang

Abstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Article
  2. Review
  3. A Protective Role of Canonical Wnt/Mediators of inflammation · 2024
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Tetraspanin-2 promotes glucotoxic apoptosis by regulating the JNK/β-catenin signaling pathway in human pancreatic β cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  9. Article
  10. Article
  11. Article
  12. IKK-β/NF-κB p65 mediates p27(Kip1) protein degradation in arsenite response.Biochemical and biophysical research communications · 2014
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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.

Dong HuDepartment of Pathology, University of Illinois at Chicago, Chicago, Illinois, United States of America.
Xiuli Bi
Wenfeng Fang
Anjia Han
Wancai Yang

Funding

Intestinal Cancer Chemoprevention: Molecular MechanismsR01CA112081 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI YANG, WANCAI · 2005 to 2009
$1.1M
NCI NIH HHS CA112081NCI NIH HHS R01 CA112081
6 · The paper itself

Abstract

backgroundWe have recently reported that mitogen-activated protein kinase (MAPK) JNK1 downregulates beta-catenin signaling and plays a critical role in regulating intestinal homeostasis and in suppressing tumor formation. This study was designed to determine whether JNK2, another MAPK, has similar and/or different functions in the regulation of beta-catenin signaling. METHODOLOGY AND PRINCIPAL

findingsWe used an in vitro system with manipulation of JNK2 and beta-catenin expression and found that activated JNK2 increased GSK3beta activity and inhibited beta-catenin expression and transcriptional activity. However, JNK2-mediated downregulation of beta-catenin was blocked by the proteasome inhibitor MG132 and GSK3beta inhibitor lithium chloride. Moreover, targeted mutations at GSK3beta phosphorylation sites (Ser33 and Ser37) of beta-catenin abrogated JNK2-mediated suppression of beta-catenin. In vivo studies further revealed that JNK2 deficiency led to upregulation of beta-catenin and increase of GSK3-beta phosphorylation in JNK2-/- mouse intestinal epithelial cells. Additionally, physical interaction and co-localization among JNK2, beta-catenin and GSK3beta were observed by immunoprecipitation, mammalian two-hybridization assay and confocal microscopy, respectively. CONCLUSION AND SIGNIFICANCE: In general, our data suggested that JNK2, like JNK1, interacts with and suppresses beta-catenin signaling in vitro and in vivo, in which GSK3beta plays a key role, although previous studies have shown distinct functions of JNK1 and JNK2. Our study also provides a novel insight into the crosstalk between Wnt/beta-catenin and MAPK JNKs signaling.

Indexed as

Animalsbeta CateninBlotting, WesternCell LineCyclin-Dependent Kinase 4Down-RegulationEnzyme InhibitorsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansImmunoprecipitationLeupeptinsMiceMice, KnockoutMitogen-Activated Protein Kinase 9Phosphorylationbenzyloxycarbonylleucyl-leucyl-leucine aldehydebeta CateninCyclin-Dependent Kinase 4Enzyme InhibitorsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, mouseLeupeptinsMitogen-Activated Protein Kinase 9

Identifiers

PMID19675674
PMCPMC2721980

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Registered trials

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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.