Evidence map›Paper›PMID 16199887›Full record

ArticleMolecular and cellular biology2005

SOCS2 can enhance interleukin-2 (IL-2) and IL-3 signaling by accelerating SOCS3 degradation.

Gillian M Tannahill, Joanne Elliott, Anna C Barry, Linda Hibbert, Nicolas A Cacalano, James A Johnston

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 147 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. SOCS2 regulates alveolar bone loss in Aggregatibacter actinomycetemcomitans-induced periodontal disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  13. Role of SOCS and VHL Proteins in Neuronal Differentiation and Development.International journal of molecular sciences · 2023
    Review
  14. International journal of molecular sciences · 2022
    Article
  15. Review
  16. Article
  17. Article
  18. Assessment of Expression ofFrontiers in immunology · 2021
    Article
  19. Review
  20. Article

11 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 2 countries.

Gillian M TannahillInfection and Immunity Group, Centre for Cancer Research and Cell Biology, Queens University, Belfast, UK.
Joanne Elliott
Anna C Barry
Linda Hibbert
Nicolas A Cacalano
James A Johnston
Queen's University Belfast · GBGenetic Information Research Institute · USOklahoma State University Center for Health Sciences · US

Funding

Wellcome Trust
6 · The paper itself

Abstract

Cytokine responses can be regulated by a family of proteins termed suppressors of cytokine signaling (SOCS) which can inhibit the JAK/STAT pathway in a classical negative-feedback manner. While the SOCS are thought to target signaling intermediates for degradation, relatively little is known about how their turnover is regulated. Unlike other SOCS family members, we find that SOCS2 can enhance interleukin-2 (IL-2)- and IL-3-induced STAT phosphorylation following and potentiate proliferation in response to cytokine stimulation. As a clear mechanism for these effects, we demonstrate that expression of SOCS2 results in marked proteasome-dependent reduction of SOCS3 and SOCS1 protein expression. Furthermore, we provide evidence that this degradation is dependent on the presence of an intact SOCS box and that the loss of SOCS3 is enhanced by coexpression of elongin B/C. This suggests that SOCS2 can bind to SOCS3 and elongin B/C to form an E3 ligase complex resulting in the degradation of SOCS3. Therefore, SOCS2 can enhance cytokine responses by accelerating proteasome-dependent turnover of SOCS3, suggesting a mechanism for the gigantism observed in SOCS2 transgenic mice.

Indexed as

AnimalsBase SequenceCell LineDNA, ComplementaryHumansInterleukin-2Interleukin-3In Vitro TechniquesMiceMice, TransgenicPhosphorylationRecombinant ProteinsRNA, MessengerSignal TransductionSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling ProteinsDNA, ComplementaryInterleukin-2Interleukin-3Recombinant ProteinsRNA, MessengerSOCS2 protein, humanSocs2 protein, mouseSOCS3 protein, humanSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling Proteins

Identifiers

PMID16199887
PMCPMC1265772
OpenAlexW2096498130

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.