Please use this identifier to cite or link to this item: http://dx.doi.org/10.25673/37177
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dc.contributor.authorBilling, Ulrike-
dc.contributor.authorJetka, Tomasz-
dc.contributor.authorNortmann, Lukas-
dc.contributor.authorWundrack, Nicole-
dc.contributor.authorKomorowski, Michal-
dc.contributor.authorWaldherr, Steffen-
dc.contributor.authorSchaper, Fred-
dc.contributor.authorDittrich, Anna-
dc.date.accessioned2021-06-30T08:51:36Z-
dc.date.available2021-06-30T08:51:36Z-
dc.date.issued2019-
dc.date.submitted2019-
dc.identifier.urihttps://opendata.uni-halle.de//handle/1981185920/37412-
dc.identifier.urihttp://dx.doi.org/10.25673/37177-
dc.description.abstractCellular 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-tocell 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.eng
dc.description.sponsorshipOVGU-Publikationsfonds 2019-
dc.language.isoeng-
dc.relation.ispartofhttps://www.nature.com/commsbio/-
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/-
dc.subjectCellular communicationeng
dc.subjectJAK/STAT signallingeng
dc.subject.ddc570-
dc.titleRobustness and information transfer within IL-6-induced JAK/STAT signallingeng
dc.typeArticle-
dc.identifier.urnurn:nbn:de:gbv:ma9:1-1981185920-374125-
local.versionTypepublishedVersion-
local.bibliographicCitation.journaltitleCommunications biology-
local.bibliographicCitation.volume2-
local.bibliographicCitation.issue2019-
local.bibliographicCitation.pagestart1-
local.bibliographicCitation.pageend14-
local.bibliographicCitation.publishernameSpringer Nature-
local.bibliographicCitation.publisherplaceLondon-
local.bibliographicCitation.doi10.1038/s42003-018-0259-4-
local.openaccesstrue-
dc.identifier.ppn1047093650-
local.bibliographicCitation.year2019-
cbs.sru.importDate2021-06-30T08:44:39Z-
local.bibliographicCitationEnthalten in Communications biology - London : Springer Nature, 2018-
local.accessrights.dnbfree-
Appears in Collections:Fakultät für Naturwissenschaften (OA)

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