Evidence map›Paper›PMID 22692453›Full record

ArticleMucosal immunology2012

IFN-γ and TNF-α-induced GBP-1 inhibits epithelial cell proliferation through suppression of β-catenin/TCF signaling.

C T Capaldo, N Beeman, R S Hilgarth, P Nava, N A Louis, E Naschberger, M Stürzl, C A Parkos, A Nusrat

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

39 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Highlights on the Contribution of Gut Microbiota to Immune-Mediated Diseases in Childhood.Mediterranean journal of hematology and infectious diseases · 2026
    Review
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  4. Article
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  12. Review
  13. Review
  14. Article
  15. Frontiers in cellular and infection microbiology · 2020
    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

9 authors at 2 institutions in 2 countries.

C T CapaldoEpithelial Pathobiology Research Unit, Department of Pathology and Laboratory of Medicine, Emory University, Atlanta, GA, USA.
N Beeman
R S Hilgarth
P Nava
N A Louis
E Naschberger
M Stürzl
C A Parkos
A Nusrat
Emory University · USFriedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

Regulation of intestinal epithelial barrier function by intercellular junction proteins in health and diseaseR01DK059888 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ASMA NUSRAT · 2001 to 2026
$10.5M
Intestinal Mucosal Wound Resealing in IBDR01DK055679 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ASMA NUSRAT · 2004 to 2026
$8.1M
Intestinal Inflammation: Signaling proteins and the rate of PMN transmigrationR01DK079392 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PARKOS, CHARLES A · 2007 to 2025
$7.2M
Neutrophil Interactions with Intestinal Epithelial CellsR01DK072564 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PARKOS, CHARLES A · 2005 to 2020
$6.5M
Structure-Function Studies on Intestinal Epithelial JAMR01DK061379 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PARKOS, CHARLES A · 2002 to 2021
$6.3M
Emory Epithelial Pathobiology Research Development CenterR24DK064399 · NIDDK · EMORY UNIVERSITY · PI PARKOS, CHARLES A · 2003 to 2012
$5.3M
INTESTINAL MUCOSAL WOUND RESEALING IN SURGICAL DISEASESR29DK055679 · NIDDK · EMORY UNIVERSITY · PI NUSRAT, ASMA · 1998 to 2002
$324k
NIDDK NIH HHS DK55679NIDDK NIH HHS DK59888NIDDK NIH HHS DK64399NIDDK NIH HHS R01 DK055679NIDDK NIH HHS R01 DK059888NIDDK NIH HHS R01 DK061379NIDDK NIH HHS R01 DK072564NIDDK NIH HHS R01 DK079392NIDDK NIH HHS R24 DK064399NIDDK NIH HHS R29 DK055679
6 · The paper itself

Abstract

Proinflammatory cytokines induce guanylate-binding protein 1 (GBP-1) protein expression in intestinal epithelial tissues. GBP-1 has been described as influencing a number of cellular processes important for epithelial homeostasis, including cell proliferation. However, many questions remain as to the role of GBP-1 in intestinal mucosal homeostasis. We therefore sought to investigate the function of proinflammatory cytokine-induced GBP-1 during intestinal epithelial cell proliferation. Through the use of complementary GBP-1 overexpression and small interfering RNA-mediated knockdown studies, we now show that GBP-1 acts to inhibit pro-mitogenic β-catenin/T cell factor (TCF) signaling. Interestingly, proinflammatory cytokine-induced GBP-1 was found to be a potent suppressor of β-catenin protein levels and β-catenin serine 552 phosphorylation. Neither glycogen synthase kinase 3β nor proteasomal inhibition alleviated GBP-1-mediated suppression of cell proliferation or β-catenin/TCF signaling, indicating a non-canonical mechanism of β-catenin inhibition. Together, these data show that cytokine-induced GBP-1 retards cell proliferation by forming a negative feedback loop that suppresses β-catenin/TCF signaling.

Indexed as

beta CateninCell Line, TumorCell ProliferationEpithelial CellsFeedback, PhysiologicalGene ExpressionGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGTP-Binding ProteinsHumansInterferon-gammaIntestinal MucosaPhosphorylationProteasome Endopeptidase ComplexProtein Kinase InhibitorsRNA, Small Interferingbeta CateninCTNNB1 protein, humanGBP1 protein, humanGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGTP-Binding ProteinsInterferon-gammaProteasome Endopeptidase ComplexProtein Kinase InhibitorsRNA, Small InterferingSerineTCF Transcription FactorsTumor Necrosis Factor-alpha

Identifiers

PMID22692453
PMCPMC3481006
OpenAlexW1552097299

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.