Show simple item record

dc.contributor.authorWells, Christineen_US
dc.contributor.authorChalk, Alistairen_US
dc.contributor.authorForrest, Alistairen_US
dc.contributor.authorTaylor, Darrinen_US
dc.contributor.authorWaddell, Nicen_US
dc.contributor.authorSchroder, Kateen_US
dc.contributor.authorHimes, S Royen_US
dc.contributor.authorFaulkner, Geoffreyen_US
dc.contributor.authorLo, Yu-Lan Sandraen_US
dc.contributor.authorKasukawa, Takeyaen_US
dc.contributor.authorKawaji, Hideyaen_US
dc.contributor.authorKai, Chikatoshien_US
dc.contributor.authorKawai, Junen_US
dc.contributor.authorKatayama, Shintaroen_US
dc.contributor.authorCarninci, Pieroen_US
dc.contributor.authorHayashizaki, Yoshihideen_US
dc.contributor.authorHume, Daviden_US
dc.contributor.authorGrimmond, Seanen_US
dc.date.accessioned2017-06-15T12:30:44Z
dc.date.available2017-06-15T12:30:44Z
dc.date.issued2006en_US
dc.date.modified2011-05-04T09:49:22Z
dc.identifier.issn1474760Xen_US
dc.identifier.doi10.1186/gb-2006-7-2-r10en_AU
dc.identifier.urihttp://hdl.handle.net/10072/12421
dc.description.abstractBACKGROUND : Alternate splicing of key signaling molecules in the Toll-like receptor (Tlr) cascade has been shown to dramatically alter the signaling capacity of inflammatory cells, but it is not known how common this mechanism is. We provide transcriptional evidence of widespread alternate splicing in the Toll-like receptor signaling pathway, derived from a systematic analysis of the FANTOM3 mouse data set. Functional annotation of variant proteins was assessed in light of inflammatory signaling in mouse primary macrophages, and the expression of each variant transcript was assessed by splicing arrays. RESULTS : A total of 256 variant transcripts were identified, including novel variants of Tlr4, Ticam1, Tollip, Rac1, Irak1, 2 and 4, Mapk14/p38, Atf2 and Stat1. The expression of variant transcripts was assessed using custom-designed splicing arrays. We functionally tested the expression of Tlr4 transcripts under a range of cytokine conditions via northern and quantitative real-time polymerase chain reaction. The effects of variant Mapk14/p38 protein expression on macrophage survival were demonstrated. CONCLUSION : Members of the Toll-like receptor signaling pathway are highly alternatively spliced, producing a large number of novel proteins with the potential to functionally alter inflammatory outcomes. These variants are expressed in primary mouse macrophages in response to inflammatory mediators such as interferon-gamma and lipopolysaccharide. Our data suggest a surprisingly common role for variant proteins in diversification/repression of inflammatory signaling.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_AU
dc.format.extent718155 bytes
dc.format.extent64072 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.languageEnglishen_US
dc.language.isoen_AU
dc.publisherBioMed Central Ltden_US
dc.publisher.placeEnglanden_US
dc.publisher.urihttp://genomebiology.com/contenten_AU
dc.relation.ispartofstudentpublicationNen_AU
dc.relation.ispartofpagefrom1en_US
dc.relation.ispartofpageto17en_US
dc.relation.ispartofjournalGenome Biologyen_US
dc.relation.ispartofvolume7en_US
dc.rights.retentionYen_AU
dc.subject.fieldofresearchcode270206en_US
dc.titleAlternate transcription of the Toll-like receptor signaling cascadeen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
dcterms.licensehttp://creativecommons.org/licenses/by/2.0en_US
gro.description.notepublicPage numbers are not for citation purposes. Instead, this article has the unique article number of R10.en_AU
gro.rights.copyrightCopyright 2006 Wells et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.en_AU
gro.date.issued2006
gro.hasfulltextFull Text


Files in this item

This item appears in the following Collection(s)

  • Journal articles
    Contains articles published by Griffith authors in scholarly journals.

Show simple item record