Evidence map›Paper›PMID 18348982›Full record

ArticleThe Journal of biological chemistry2008

Differential regulation of the IL-17 receptor by gammac cytokines: inhibitory signaling by the phosphatidylinositol 3-kinase pathway.

Matthew J Lindemann, Zihua Hu, Marta Benczik, Kathleen D Liu, Sarah L Gaffen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
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  10. Article
  11. The effect of proinflammatory cytokines on IL-17RA expression in NSCLC.Medical oncology (Northwood, London, England) · 2014
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. IL-17 signaling in host defense and inflammatory diseases.Cellular & molecular immunology · 2010
    Review
  17. The IL-17 family cytokines in immunity and disease.Journal of clinical immunology · 2010
    Review
  18. Review
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 2 institutions in 1 country.

Matthew J LindemannDepartment of Oral Biology, University at Buffalo, State University of New York, Buffalo, New York 14214, USA.
Zihua Hu
Marta Benczik
Kathleen D Liu
Sarah L Gaffen
University at Buffalo, State University of New York · USUniversity of California, San Francisco · US

Funding

INTERLEUKIN-17 RECEPTOR SIGNALING IN BONER21AR050458 · NIAMS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI GAFFEN, SARAH L. · 2005 to 2006
$309k
TITANIUM ALLOYS FOR PARTIAL DENTURESR43DE007034 · NIDCR · GREENMARK, INC. · PI MARKER, BERNARD C · 1985 to 1985
–
NIAID NIH HHS AI05439NIAMS NIH HHS AR050458NIDCR NIH HHS DE007034
6 · The paper itself

Abstract

The gammac-family cytokine IL-2 activates signaling events that contribute to cell survival and proliferation, the best-studied of which are the STAT-5 and phosphatidylinositol 3-kinase (PI3K) pathways. The starting point of this study was to define genes regulated by the IL-2R-mediated PI3K pathway in T cells. Accordingly, we used an erythropoietin (EPO) receptor chimeric receptor system in which IL-2-dependent HT-2 T cells expressed a mutant EPO-IL-2Rbeta construct where Tyr-338 is mutated to Phe. Cells expressing this mutant IL-2Rbeta chain fail to induce phosphorylation of PI3K-p85alpha/beta or activate Akt, but mediate normal IL-2-dependent proliferation and activation of JAK1 and STAT-5A/B. Microarray analyses revealed differential regulation of numerous genes compared with cells expressing a wild-type IL-2Rbeta, including up-regulation of the IL-17 receptor subunit IL-17RA. Blockade of the PI3K pathway but not p70S6K led to up-regulation of IL-17RA, and constitutive Akt activation was associated with suppressed IL-17RA expression. Moreover, similar to the mutant EPO-IL-2Rbeta chimera, IL-15 and IL-21 induced IL-17RA preferentially compared with IL-2, and IL-2 but not IL-15 or IL-21 mediated prolonged activation of the PI3K p85 regulatory subunit. Thus, there are intrinsic signaling differences between IL-2 and IL-15 that can be attributed to differences in activation of the PI3K pathway.

Indexed as

Gene Expression RegulationCell ProliferationCytokinesGene Expression Regulation, EnzymologicHumansInterleukin-2Jurkat CellsModels, BiologicalMutationOligonucleotide Array Sequence AnalysisPhosphatidylinositol 3-KinasesPhosphorylationReceptors, Interleukin-17Signal TransductionSTAT5 Transcription FactorTumor Suppressor ProteinsCytokinesInterleukin-2Phosphatidylinositol 3-KinasesReceptors, Interleukin-17STAT5A protein, humanSTAT5 Transcription FactorTumor Suppressor Proteins

Identifiers

PMID18348982
PMCPMC2376247
OpenAlexW2074170748

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.