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Meininger, I. ; Griesbach, R.A. ; Hu, D. ; Gehring, T. ; Seeholzer, T. ; Bertossi, A. ; Kranich, J.* ; Oeckinghaus, A. ; Eitelhuber, A.C. ; Greczmiel, U. ; Gewies, A.* ; Schmidt-Supprian, M.* ; Ruland, J.* ; Brocker, T.* ; Heissmeyer, V. ; Heyd, F.* ; Krappmann, D.

Alternative splicing of MALT1 controls signalling and activation of CD4+ T cells.

Nat. Commun. 7:11292 (2016)
Publ. Version/Full Text Supplement DOI PMC
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MALT1 channels proximal T-cell receptor (TCR) signalling to downstream signalling pathways. With MALT1A and MALT1B two conserved splice variants exist and we demonstrate here that MALT1 alternative splicing supports optimal T-cell activation. Inclusion of exon7 in MALT1A facilitates the recruitment of TRAF6, which augments MALT1 scaffolding function, but not protease activity. Naive CD4(+) T cells express almost exclusively MALT1B and MALT1A expression is induced by TCR stimulation. We identify hnRNP U as a suppressor of exon7 inclusion. Whereas selective depletion of MALT1A impairs T-cell signalling and activation, downregulation of hnRNP U enhances MALT1A expression and T-cell activation. Thus, TCR-induced alternative splicing augments MALT1 scaffolding to enhance downstream signalling and to promote optimal T-cell activation.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Nf-kappa-b; Paracaspase Malt1; Immune Cells; Ubiquitin Chains; Hnrnp L; Inflammation; Cleavage; Lymphocytes; Regulator; Infection
Language english
Publication Year 2016
HGF-reported in Year 2016
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Journal Nature Communications
Quellenangaben Volume: 7, Issue: , Pages: , Article Number: 11292 Supplement: ,
Publisher Nature Publishing Group
Publishing Place London
Reviewing status Peer reviewed
Institute(s) Research Unit Signaling and Translation (SAT)
Research Unit Molecular Immune Regulation (AMIR)
POF-Topic(s) 30203 - Molecular Targets and Therapies
Research field(s) Enabling and Novel Technologies
Immune Response and Infection
PSP Element(s) G-509800-002
G-501712-001
PubMed ID 27068814
DOI 10.1038/ncomms11292
WOS ID WOS:000373831500001
Scopus ID 84964335701
Erfassungsdatum 2016-04-18
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