Evidence map›Paper›PMID 11709700›Full record

ArticleOncogene2001

Induction of the IL-13 receptor alpha2-chain by IL-4 and IL-13 in human keratinocytes: involvement of STAT6, ERK and p38 MAPK pathways.

M David, D Ford, J Bertoglio, A L Maizel, J Pierre

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. The Central Roles of Keratinocytes in Coordinating Skin Immunity.The Journal of investigative dermatology · 2024
    Review
  5. Article
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  9. Modulation of IL-4/IL-13 cytokine signaling in the context of allergic disease.The Journal of allergy and clinical immunology · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Igalan from Inula helenium (L.) suppresses the atopic dermatitis-like response in stimulated HaCaT keratinocytes via JAK/STAT3 signaling.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
    Article
  15. Article
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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 4 institutions in 2 countries.

M DavidINSERM U461, Faculte de Pharmacie, 5, rue JB Clement, 92296 Chatenay Malabry Cedex, France.
D Ford
J Bertoglio
A L Maizel
J Pierre
Boston University · USInserm · FRLaboratoire d'Énergétique Moléculaire et Macroscopique, Combustion · FRProvidence College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IL-4 and IL-13 are related cytokines which induce both pro- and anti-inflammatory effects depending on the cell type they act upon and the nature of the receptors expressed. The type I receptor complex is composed of the IL-4Ralpha and gammac and only binds IL-4, whereas, in the type II receptor, IL-4Ralpha dimerizes with IL-13Ralpha1 upon either IL-4 or IL-13 binding. Another ligand binding chain potentially implicated in the IL-4/IL-13 receptor has been described, the IL-13Ralpha2, but the regulation of its expression and its role in IL-4/IL-13 transduction is poorly understood. In this study we report that IL-4 and IL-13 upregulate IL-13Ralpha2 at both the mRNA and protein levels in the keratinocyte cell line HaCaT. In these cells, IL-4 or IL-13 were shown to activate the Janus Kinases JAK1 and JAK2, the transcription factor STAT6, and the ERK and p38 mitogen-activated protein kinases. We show that IL-4 or IL-13-induced IL-13Ralpha2 mRNA expression was inhibited by the ERK inhibitor U0126, the JAK inhibitor AG490 and, to a lesser extent, the p38 MAPK inhibitor SB203580. Moreover, expression of a constitutive active mutant of STAT6 alone did not modify IL-13Ralpha2 mRNA expression, but potentiated the effects of IL-4 or IL-13 on IL-13Ralpha2 expression. The constitutive active mutants of MEK1 or MKK6 increased the level of expression of IL-13Ralpha2 mRNA even in absence of stimulation. Our findings demonstrate, for the first time, that IL-4 and IL-13 can induce IL-13Ralpha2 expression in keratinocytes, and that the ERK and p38 MAPK together with JAK2 and STAT6 play a critical role in this process.

Indexed as

Gene Expression Regulation, NeoplasticAntineoplastic AgentsBlotting, WesternButadienesCross-Linking ReagentsEnzyme InhibitorsImidazolesInterleukin-13Interleukin-13 Receptor alpha1 SubunitInterleukin-4KeratinocytesKineticsLigandsMitogen-Activated Protein KinasesNitrilesp38 Mitogen-Activated Protein Kinasesalpha-cyano-(3,4-dihydroxy)-N-benzylcinnamideAntineoplastic AgentsButadienesCross-Linking ReagentsEnzyme InhibitorsIL13RA1 protein, humanImidazolesInterleukin-13Interleukin-13 Receptor alpha1 SubunitInterleukin-4LigandsMitogen-Activated Protein KinasesNitrilesp38 Mitogen-Activated Protein KinasesPyridinesReceptors, InterleukinReceptors, Interleukin-13RNA, MessengerSB 203580STAT6 Transcription FactorTrans-ActivatorsTyrphostinsU 0126

Identifiers

PMID11709700
OpenAlexW1964464038

What OpenQuestion holds

Textmetadata
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.