Evidence map›Paper›PMID 30675525›Full record

ArticleCommunications biology2019

Robustness and Information Transfer within IL-6-induced JAK/STAT Signalling.

Ulrike Billing, Tomasz Jetka, Lukas Nortmann, Nicole Wundrack, Michal Komorowski, Steffen Waldherr, Fred Schaper, Anna Dittrich

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

38 citing papers in PubMed, 62 citations in OpenAlex.

  1. Combination of PARP Inhibitor Olaparib, and PD-L1 Inhibitor Durvalumab, in Recurrent Ovarian Cancer: a Proof-of-Concept Phase II Study.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
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  14. A Review on Role of Inflammation in Coronavirus Disease.Endocrine, metabolic & immune disorders drug targets · 2024
    Review
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  16. Article
  17. 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

8 authors at 3 institutions in 3 countries.

Ulrike Billing1Otto-von-Guericke University Magdeburg, Institute of Biology, Department of Systems Biology, Universitätsplatz 2, 39106 Magdeburg, Germany.ORCID 0000-0003-0538-0180
Tomasz JetkaPolish Academy of Sciences, Institute of Fundamental Technological Research, Division of Modelling in Biology and Medicine, Pawinskiego 5B, 02- 106, Warszawa, Poland.
Lukas Nortmann1Otto-von-Guericke University Magdeburg, Institute of Biology, Department of Systems Biology, Universitätsplatz 2, 39106 Magdeburg, Germany.ORCID 0000-0002-1117-0932
Nicole Wundrack1Otto-von-Guericke University Magdeburg, Institute of Biology, Department of Systems Biology, Universitätsplatz 2, 39106 Magdeburg, Germany.ORCID 0000-0003-0894-8448
Michal KomorowskiPolish Academy of Sciences, Institute of Fundamental Technological Research, Division of Modelling in Biology and Medicine, Pawinskiego 5B, 02- 106, Warszawa, Poland.
Steffen WaldherrKU Leuven, Department of Chemical Engineering, Celestijnenlaan 200f - box 2424, 3001 Leuven, Belgium.ORCID 0000-0002-0936-579X
Fred Schaper1Otto-von-Guericke University Magdeburg, Institute of Biology, Department of Systems Biology, Universitätsplatz 2, 39106 Magdeburg, Germany.ORCID 0000-0002-8899-5414
Anna Dittrich1Otto-von-Guericke University Magdeburg, Institute of Biology, Department of Systems Biology, Universitätsplatz 2, 39106 Magdeburg, Germany.ORCID 0000-0002-1056-4219
Otto-von-Guericke-Universität Magdeburg · DEInstitute of Fundamental Technological Research · PLKU Leuven · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular communication via intracellular signalling pathways is crucial. Expression and activation of signalling proteins is heterogenous between isogenic cells of the same cell-type. However, mechanisms evolved to enable sufficient communication and to ensure cellular functions. We use information theory to clarify mechanisms facilitating IL-6-induced JAK/STAT signalling despite cell-to-cell variability. We show that different mechanisms enabling robustness against variability complement each other. Early STAT3 activation is robust as long as cytokine concentrations are low. Robustness at high cytokine concentrations is ensured by high STAT3 expression or serine phosphorylation. Later the feedback-inhibitor SOCS3 increases robustness. Channel Capacity of JAK/STAT signalling is limited by cell-to-cell variability in STAT3 expression and is affected by the same mechanisms governing robustness. Increasing STAT3 amount increases Channel Capacity and robustness, whereas increasing STAT3 tyrosine phosphorylation reduces robustness but increases Channel Capacity. In summary, we elucidate mechanisms preventing dysregulated signalling by enabling reliable JAK/STAT signalling despite cell-to-cell heterogeneity.

Indexed as

Signal TransductionAnimalsCell LineCytokinesDose-Response Relationship, DrugFibroblastsGene Expression RegulationInterleukin-6Janus KinasesMicePhosphorylationSTAT3 Transcription FactorSTAT Transcription FactorsSuppressor of Cytokine Signaling 3 ProteinCytokinesInterleukin-6Janus KinasesSTAT3 Transcription FactorSTAT Transcription FactorsSuppressor of Cytokine Signaling 3 Protein

Identifiers

PMID30675525
PMCPMC6338669
OpenAlexW2910137290

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.