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Article: Coronin-1A links cytoskeleton dynamics to TCRαβ-induced cell signaling

TitleCoronin-1A links cytoskeleton dynamics to TCRαβ-induced cell signaling
Authors
Issue Date2008
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
Plos One, 2008, v. 3 n. 10 How to Cite?
AbstractActin polymerization plays a critical role in activated T lymphocytes both in regulating T cell receptor (TCR)-induced immunological synapse (IS) formation and signaling. Using gene targeting, we demonstrate that the hematopoietic specific, actin- and Arp2/3 complex-binding protein coronin-1A contributes to both processes. Coronin-1A-deficient mice specifically showed alterations in terminal development and the survival of αβT cells, together with defects in cell activation and cytokine production following TCR triggering. The mutant T cells further displayed excessive accumulation yet reduced dynamics of F-actin and the WASP-Arp2/3 machinery at the IS, correlating with extended cell-cell contact. Cell signaling was also affected with the basal activation of the stress kinases sAPK/JNK1/2; and deficits in TCR-induced Ca 2+ influx and phosphorylation and degradation of the inhibitor of NF-κB (IκB). Coronin-1A therefore links cytoskeleton plasticity with the functioning of discrete TCR signaling components. This function may be required to adjust TCR responses to selecting ligands accounting in part for the homeostasis defect that impacts αβT cells in coronin-1A deficient mice, with the exclusion of other lympho/hematopoietic lineages. © 2008 Mugnier et al.
Persistent Identifierhttp://hdl.handle.net/10722/60593
ISSN
2015 Impact Factor: 3.057
2015 SCImago Journal Rankings: 1.395
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Inserm
CNRS
Association pour la Recherche sur le Cancer (ARC)fellowship
Fondation Princesse Grace de Monaco
Commission of the European Communities
Ministere de l'Education Nationale et de la RechercheACI #108
Ligue Nationale Contre le Cancerfellowship
Funding Information:

This work was supported by Inserm, CNRS, the Association pour la Recherche sur le Cancer (ARC), the Fondation Princesse Grace de Monaco, and the Commission of the European Communities (to PF); and from the Ministere de l'Education Nationale et de la Recherche (ACI #108) (to PF and AA). BN was supported by fellowships from the Ligue Nationale Contre le Cancer and ARC. BM was supported by a fellowship from ARC.

References

 

DC FieldValueLanguage
dc.contributor.authorMugnier, Ben_HK
dc.contributor.authorNal, Ben_HK
dc.contributor.authorVerthuy, Cen_HK
dc.contributor.authorBoyer, Cen_HK
dc.contributor.authorLam, Den_HK
dc.contributor.authorChasson, Len_HK
dc.contributor.authorNieoullon, Ven_HK
dc.contributor.authorChazal, Gen_HK
dc.contributor.authorGuo, XJen_HK
dc.contributor.authorHe, HTen_HK
dc.contributor.authorRueffJuy, Den_HK
dc.contributor.authorAlcover, Aen_HK
dc.contributor.authorFerrier, Pen_HK
dc.date.accessioned2010-05-31T04:14:26Z-
dc.date.available2010-05-31T04:14:26Z-
dc.date.issued2008en_HK
dc.identifier.citationPlos One, 2008, v. 3 n. 10en_HK
dc.identifier.issn1932-6203en_HK
dc.identifier.urihttp://hdl.handle.net/10722/60593-
dc.description.abstractActin polymerization plays a critical role in activated T lymphocytes both in regulating T cell receptor (TCR)-induced immunological synapse (IS) formation and signaling. Using gene targeting, we demonstrate that the hematopoietic specific, actin- and Arp2/3 complex-binding protein coronin-1A contributes to both processes. Coronin-1A-deficient mice specifically showed alterations in terminal development and the survival of αβT cells, together with defects in cell activation and cytokine production following TCR triggering. The mutant T cells further displayed excessive accumulation yet reduced dynamics of F-actin and the WASP-Arp2/3 machinery at the IS, correlating with extended cell-cell contact. Cell signaling was also affected with the basal activation of the stress kinases sAPK/JNK1/2; and deficits in TCR-induced Ca 2+ influx and phosphorylation and degradation of the inhibitor of NF-κB (IκB). Coronin-1A therefore links cytoskeleton plasticity with the functioning of discrete TCR signaling components. This function may be required to adjust TCR responses to selecting ligands accounting in part for the homeostasis defect that impacts αβT cells in coronin-1A deficient mice, with the exclusion of other lympho/hematopoietic lineages. © 2008 Mugnier et al.en_HK
dc.languageengen_HK
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_HK
dc.relation.ispartofPLoS ONEen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshCytoskeleton - metabolism-
dc.subject.meshHomeostasis-
dc.subject.meshMicrofilament Proteins - physiology-
dc.subject.meshReceptors, Antigen, T-Cell, alpha-beta - physiology-
dc.subject.meshT-Lymphocytes - cytology-
dc.titleCoronin-1A links cytoskeleton dynamics to TCRαβ-induced cell signalingen_HK
dc.typeArticleen_HK
dc.identifier.emailNal, B: bnal@hkucc.hku.hken_HK
dc.identifier.authorityNal, B=rp00541en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0003467en_HK
dc.identifier.pmid18941544-
dc.identifier.pmcidPMC2568942-
dc.identifier.scopuseid_2-s2.0-54949156418en_HK
dc.identifier.hkuros162664en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-54949156418&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume3en_HK
dc.identifier.issue10en_HK
dc.identifier.spagee3467-
dc.identifier.epagee3467-
dc.identifier.isiWOS:000265125900011-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridMugnier, B=6603364015en_HK
dc.identifier.scopusauthoridNal, B=6506672380en_HK
dc.identifier.scopusauthoridVerthuy, C=6602374950en_HK
dc.identifier.scopusauthoridBoyer, C=7202036033en_HK
dc.identifier.scopusauthoridLam, D=7201749626en_HK
dc.identifier.scopusauthoridChasson, L=16028136000en_HK
dc.identifier.scopusauthoridNieoullon, V=8512244100en_HK
dc.identifier.scopusauthoridChazal, G=6603058116en_HK
dc.identifier.scopusauthoridGuo, XJ=7404330130en_HK
dc.identifier.scopusauthoridHe, HT=55214926600en_HK
dc.identifier.scopusauthoridRueffJuy, D=6701680836en_HK
dc.identifier.scopusauthoridAlcover, A=7004078232en_HK
dc.identifier.scopusauthoridFerrier, P=7006480116en_HK

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