| First Author | Meininger I | Year | 2016 |
| Journal | Nat Commun | Volume | 7 |
| Pages | 11292 | PubMed ID | 27068814 |
| Mgi Jnum | J:236892 | Mgi Id | MGI:5810048 |
| Doi | 10.1038/ncomms11292 | Citation | Meininger I, et al. (2016) Alternative splicing of MALT1 controls signalling and activation of CD4(+) T cells. Nat Commun 7:11292 |
| abstractText | 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. |
