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dc.contributor.authorMorris, O
dc.contributor.authorLiu, X
dc.contributor.authorDomingues, C
dc.contributor.authorRunchel, C
dc.contributor.authorChai, A
dc.contributor.authorBasith, S
dc.contributor.authorTenev, T
dc.contributor.authorChen, H
dc.contributor.authorChoi, S
dc.contributor.authorPennetta, G
dc.contributor.authorBuchon, N
dc.contributor.authorMeier, P
dc.date.accessioned2016-09-28T13:27:25Z
dc.date.issued2016-09
dc.identifier.citationCell host & microbe, 2016, 20 (3), pp. 283 - 295
dc.identifier.issn1931-3128
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/143
dc.identifier.eissn1934-6069
dc.identifier.doi10.1016/j.chom.2016.08.003
dc.description.abstractPattern recognition receptors are activated following infection and trigger transcriptional programs important for host defense. Tight regulation of NF-κB activation is critical to avoid detrimental and misbalanced responses. We describe Pickle, a Drosophila nuclear IκB that integrates signaling inputs from both the Imd and Toll pathways by skewing the transcriptional output of the NF-κB dimer repertoire. Pickle interacts with the NF-κB protein Relish and the histone deacetylase dHDAC1, selectively repressing Relish homodimers while leaving other NF-κB dimer combinations unscathed. Pickle's ability to selectively inhibit Relish homodimer activity contributes to proper host immunity and organismal health. Although loss of pickle results in hyper-induction of Relish target genes and improved host resistance to pathogenic bacteria in the short term, chronic inactivation of pickle causes loss of immune tolerance and shortened lifespan. Pickle therefore allows balanced immune responses that protect from pathogenic microbes while permitting the establishment of beneficial commensal host-microbe relationships.
dc.formatPrint
dc.format.extent283 - 295
dc.languageeng
dc.language.isoeng
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.subjectAnimals
dc.subjectDrosophila
dc.subjectDrosophila Proteins
dc.subjectTranscription Factors
dc.subjectProtein Interaction Mapping
dc.subjectSignal Transduction
dc.subjectProtein Binding
dc.subjectI-kappa B Proteins
dc.subjectImmunity, Innate
dc.subjectHistone Deacetylase 1
dc.titleSignal Integration by the IκB Protein Pickle Shapes Drosophila Innate Host Defense.
dc.typeJournal Article
dcterms.dateAccepted2016-08-12
rioxxterms.versionofrecord10.1016/j.chom.2016.08.003
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.licenseref.startdate2016-09
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfCell host & microbe
pubs.issue3
pubs.notes6 months
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research/Cell Death and Immunity
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research/Target Discovery & Apoptosis
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Therapeutics
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Therapeutics/Target Discovery & Apoptosis
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research/Cell Death and Immunity
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research/Target Discovery & Apoptosis
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Therapeutics
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Therapeutics/Target Discovery & Apoptosis
pubs.publication-statusPublished
pubs.volume20en_US
pubs.embargo.terms6 months
icr.researchteamCell Death and Immunityen_US
icr.researchteamTarget Discovery & Apoptosisen_US
dc.contributor.icrauthorMeier, Pascalen
dc.contributor.icrauthorMorris, Ottoen
dc.contributor.icrauthorRunchel, Christopheren


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