Evidence map›Paper›PMID 31238931›Full record

ArticleCell communication and signaling : CCS2019

Intragenic regulation of SOCS3 isoforms.

Oliver Klepsch, Lise Sarah Namer, Nadine Köhler, Raymond Kaempfer, Anna Dittrich, Fred Schaper

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. YTHDF1 Negatively RegulatesFrontiers in immunology · 2022
    Article
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  6. Article
  7. 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

6 authors at 2 institutions in 2 countries.

Oliver KlepschDepartment of Systems Biology, Institute of Biology, Otto-von-Guericke University Magdeburg, Universitätsplatz 2, 39106, Magdeburg, Germany.
Lise Sarah NamerDepartment of Biochemistry and Molecular Biology, Institute of Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School, 9112102, Jerusalem, Israel.
Nadine KöhlerDepartment of Systems Biology, Institute of Biology, Otto-von-Guericke University Magdeburg, Universitätsplatz 2, 39106, Magdeburg, Germany.
Raymond KaempferDepartment of Biochemistry and Molecular Biology, Institute of Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School, 9112102, Jerusalem, Israel.
Anna DittrichDepartment of Systems Biology, Institute of Biology, Otto-von-Guericke University Magdeburg, Universitätsplatz 2, 39106, Magdeburg, Germany. anna.dittrich@ovgu.de.
Fred SchaperDepartment of Systems Biology, Institute of Biology, Otto-von-Guericke University Magdeburg, Universitätsplatz 2, 39106, Magdeburg, Germany. fred.schaper@ovgu.de.ORCID 0000-0002-8899-5414
Otto-von-Guericke-Universität Magdeburg · DEHebrew University of Jerusalem · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInflammatory reactions are commonly affected by stress responses. Interleukin-6 signalling is part of the inflammatory response and is stringently regulated by the feedback inhibitor SOCS3 expressed in a short and long isoform. Here, we studied the inhibitory potential of the two SOCS3 isoforms. Furthermore, we analysed the regulation of SOCS3 isoform expression and the role of PKR stress kinase signalling in SOCS3 protein expression.

methodsWe performed Western blotting, reporter assays, genetic analyses and manipulations for studying SOCS3 isoform expression and activation of signalling components involved in interleukin-6-induced and PKR-dependent signalling.

resultsInterleukin-6-induced endogenous expression of both SOCS3 isoforms was found in distinct cell types. Forced expression of either the long or short SOCS3 isoform demonstrated equal inhibitory activity of each isoform and confirmed longer half-life of the short isoform. Study of intragenic regulation of SOCS3 isoform expression revealed that (i) the 5'-UTR of SOCS3 mRNA restrains specifically expression of the long SOCS3 isoform, (ii) expression of the long isoform restrains expression of the short isoform, and (iii) signalling through the stress kinase PKR does not impact on SOCS3 isoform ratio.

conclusionsBoth SOCS3 isoforms show a similar potential for inhibiting interleukin-6 signalling but differ in their half-lives. Relative expression of the isoforms depends on intragenic elements yet is independent of PKR signalling.

Indexed as

Gene Expression RegulationCodonHEK293 CellsHeLa CellsHumansInterleukin-6Protein IsoformsSignal TransductionSuppressor of Cytokine Signaling 3 ProteinCodonInterleukin-6Protein IsoformsSuppressor of Cytokine Signaling 3 ProteinInterleukin-6JAKPKRSignal transductionSOCSSTATStress response

Identifiers

PMID31238931
PMCPMC6593527
OpenAlexW2953637764

What OpenQuestion holds

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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.