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Article: Coronin-1A links cytoskeleton dynamics to TCRαβ-induced cell signaling
Title | Coronin-1A links cytoskeleton dynamics to TCRαβ-induced cell signaling | ||||||||||||||||
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Authors | |||||||||||||||||
Issue Date | 2008 | ||||||||||||||||
Publisher | Public 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? | ||||||||||||||||
Abstract | Actin 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 Identifier | http://hdl.handle.net/10722/60593 | ||||||||||||||||
ISSN | 2023 Impact Factor: 2.9 2023 SCImago Journal Rankings: 0.839 | ||||||||||||||||
PubMed Central ID | |||||||||||||||||
ISI Accession Number ID |
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 Field | Value | Language |
---|---|---|
dc.contributor.author | Mugnier, B | en_HK |
dc.contributor.author | Nal, B | en_HK |
dc.contributor.author | Verthuy, C | en_HK |
dc.contributor.author | Boyer, C | en_HK |
dc.contributor.author | Lam, D | en_HK |
dc.contributor.author | Chasson, L | en_HK |
dc.contributor.author | Nieoullon, V | en_HK |
dc.contributor.author | Chazal, G | en_HK |
dc.contributor.author | Guo, XJ | en_HK |
dc.contributor.author | He, HT | en_HK |
dc.contributor.author | RueffJuy, D | en_HK |
dc.contributor.author | Alcover, A | en_HK |
dc.contributor.author | Ferrier, P | en_HK |
dc.date.accessioned | 2010-05-31T04:14:26Z | - |
dc.date.available | 2010-05-31T04:14:26Z | - |
dc.date.issued | 2008 | en_HK |
dc.identifier.citation | Plos One, 2008, v. 3 n. 10 | en_HK |
dc.identifier.issn | 1932-6203 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/60593 | - |
dc.description.abstract | Actin 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.language | eng | en_HK |
dc.publisher | Public Library of Science. The Journal's web site is located at http://www.plosone.org/home.action | en_HK |
dc.relation.ispartof | PLoS ONE | en_HK |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.subject.mesh | Cytoskeleton - metabolism | - |
dc.subject.mesh | Homeostasis | - |
dc.subject.mesh | Microfilament Proteins - physiology | - |
dc.subject.mesh | Receptors, Antigen, T-Cell, alpha-beta - physiology | - |
dc.subject.mesh | T-Lymphocytes - cytology | - |
dc.title | Coronin-1A links cytoskeleton dynamics to TCRαβ-induced cell signaling | en_HK |
dc.type | Article | en_HK |
dc.identifier.email | Nal, B: bnal@hkucc.hku.hk | en_HK |
dc.identifier.authority | Nal, B=rp00541 | en_HK |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.1371/journal.pone.0003467 | en_HK |
dc.identifier.pmid | 18941544 | - |
dc.identifier.pmcid | PMC2568942 | - |
dc.identifier.scopus | eid_2-s2.0-54949156418 | en_HK |
dc.identifier.hkuros | 162664 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-54949156418&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 3 | en_HK |
dc.identifier.issue | 10 | en_HK |
dc.identifier.spage | e3467 | - |
dc.identifier.epage | e3467 | - |
dc.identifier.isi | WOS:000265125900011 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Mugnier, B=6603364015 | en_HK |
dc.identifier.scopusauthorid | Nal, B=6506672380 | en_HK |
dc.identifier.scopusauthorid | Verthuy, C=6602374950 | en_HK |
dc.identifier.scopusauthorid | Boyer, C=7202036033 | en_HK |
dc.identifier.scopusauthorid | Lam, D=7201749626 | en_HK |
dc.identifier.scopusauthorid | Chasson, L=16028136000 | en_HK |
dc.identifier.scopusauthorid | Nieoullon, V=8512244100 | en_HK |
dc.identifier.scopusauthorid | Chazal, G=6603058116 | en_HK |
dc.identifier.scopusauthorid | Guo, XJ=7404330130 | en_HK |
dc.identifier.scopusauthorid | He, HT=55214926600 | en_HK |
dc.identifier.scopusauthorid | RueffJuy, D=6701680836 | en_HK |
dc.identifier.scopusauthorid | Alcover, A=7004078232 | en_HK |
dc.identifier.scopusauthorid | Ferrier, P=7006480116 | en_HK |
dc.identifier.issnl | 1932-6203 | - |