Evidence map›Paper›PMID 26306032›Full record

ArticleThe Journal of biological chemistry2015

Prerequisites for Functional Interleukin 31 Signaling and Its Feedback Regulation by Suppressor of Cytokine Signaling 3 (SOCS3).

Elisabeth Maier, Michaela Mittermeir, Stefanie Ess, Theresa Neuper, Angela Schmiedlechner, Albert Duschl, Jutta Horejs-Hoeck

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.1field-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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Human germline biallelic loss-of-functionJournal of human immunity · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. IL-31, itch and hematological malignancies.Clinical and molecular allergy : CMA · 2021
    Review
  10. Interleukin-31 and Pruritic Skin.Journal of clinical medicine · 2021
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. 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

7 authors at 1 institution in 1 country.

Elisabeth MaierFrom the Department of Molecular Biology, University of Salzburg, 5020 Salzburg, Austria.
Michaela MittermeirFrom the Department of Molecular Biology, University of Salzburg, 5020 Salzburg, Austria.
Stefanie EssFrom the Department of Molecular Biology, University of Salzburg, 5020 Salzburg, Austria.
Theresa NeuperFrom the Department of Molecular Biology, University of Salzburg, 5020 Salzburg, Austria.
Angela SchmiedlechnerFrom the Department of Molecular Biology, University of Salzburg, 5020 Salzburg, Austria.
Albert DuschlFrom the Department of Molecular Biology, University of Salzburg, 5020 Salzburg, Austria.
Jutta Horejs-HoeckFrom the Department of Molecular Biology, University of Salzburg, 5020 Salzburg, Austria jutta.horejs_hoeck@sbg.ac.at.
University of Salzburg · AT

Funding

Austrian Science Fund FWF P 23933Austrian Science Fund FWF P 25696
6 · The paper itself

Abstract

Interleukin-31 (IL-31) is a T helper type 2 cell-derived cytokine tightly associated with inflammatory skin disorders. IL-31-induced signaling is mediated by a receptor complex composed of oncostatin M receptor β and the cytokine-specific receptor subunit IL-31Rα, of which there are several isoforms. The latter can be classified as long or short isoforms with respect to their intracellular domain. At present, the signaling capabilities of the different isoforms remain inchoately understood, and potential mechanisms involved in negative regulation of IL-31Rα signaling have so far not been studied in detail. Here, we show that both the long and short isoforms of IL-31Rα are capable of inducing STAT signaling. However, the presence of a functional JAK-binding box within IL-31Rα is an essential prerequisite for functional IL-31-mediated STAT3 signaling. Moreover, both the long and short isoforms require oncostatin M receptor β for their activity. We also show that IL-31 induces expression of four suppressor of cytokine signaling family members and provide evidence that SOCS3 acts as a potent feedback inhibitor of IL-31-induced signaling. Taken together, this study identifies crucial requirements for IL-31 signaling and shows its counter-regulation by SOCS3.

Indexed as

Feedback, PhysiologicalSignal TransductionAmino Acid MotifsCell MembraneGene Expression RegulationHEK293 CellsHeLa CellsHumansInterleukinsIntracellular SpaceOncostatin M Receptor beta SubunitProtein IsoformsReceptors, InterleukinSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling ProteinsTyrosineIL31 protein, humanIL31RA protein, humanInterleukinsOncostatin M Receptor beta SubunitOSMR protein, humanProtein IsoformsReceptors, InterleukinSOCS3 protein, humanSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling ProteinsTyrosinefeedback inhibitionIL-31R α isoformsIL-31 signalinginterleukinOSMR βreceptorsignal transductionSTAT3suppressor of cytokine signaling 3 (SOCS3)suppressors of cytokine signaling 1 (SOCS1)

Identifiers

PMID26306032
PMCPMC4598987
OpenAlexW1846474778

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.