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T-cell receptor-induced JNK activation requires proteolytic inactivation of CYLD by MALT1

Jens Staal (UGent), Yasmine Driege (UGent), Tine Bekaert (UGent), Annelies Demeyer (UGent), David Muyllaert (UGent), Petra Van Damme (UGent), Kris Gevaert (UGent) and Rudi Beyaert (UGent)
(2011) EMBO JOURNAL. 30(9). p.1742-1752
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Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
Abstract
The paracaspase mucosa-associated lymphoid tissue 1 (MALT1) is central to lymphocyte activation and lymphomagenesis. MALT1 mediates antigen receptor signalling to NF-kappa B by acting as a scaffold protein. Furthermore, MALT1 has proteolytic activity that contributes to optimal NF-kappa B activation by cleaving the NF-kappa B inhibitor A20. Whether MALT1 protease activity is involved in other signalling pathways, and the identity of the relevant substrates, is unknown. Here, we show that T-cell receptors (TCR) activation, as well as overexpression of the oncogenic API2-MALT1 fusion protein, results in proteolytic inactivation of CYLD by MALT1, which is specifically required for c-jun N-terminal kinase (JNK) activation and the inducible expression of a subset of genes. These results indicate a novel role for MALT1 proteolytic activity in TCR-induced JNK activation and reveal CYLD cleavage as the underlying mechanism.
Keywords
signal transduction, ubiquitination, NF-KAPPA-B, UBIQUITIN-DEPENDENT KINASE, CYTOKINE PRODUCTION, DEUBIQUITINATING ENZYME CYLD, TUMOR-SUPPRESSOR CYLD, CARMA3/BCL10/MALT1 COMPLEX, SIGNALING PATHWAY, NEGATIVE REGULATION, TAK1, PROTEIN, MAP kinase, cytokine, AP-1

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Chicago
Staal, Jens, Yasmine Driege, Tine Bekaert, Annelies Demeyer, David Muyllaert, Petra Van Damme, Kris Gevaert, and Rudi Beyaert. 2011. “T-cell Receptor-induced JNK Activation Requires Proteolytic Inactivation of CYLD by MALT1.” Embo Journal 30 (9): 1742–1752.
APA
Staal, J., Driege, Y., Bekaert, T., Demeyer, A., Muyllaert, D., Van Damme, P., Gevaert, K., et al. (2011). T-cell receptor-induced JNK activation requires proteolytic inactivation of CYLD by MALT1. EMBO JOURNAL, 30(9), 1742–1752.
Vancouver
1.
Staal J, Driege Y, Bekaert T, Demeyer A, Muyllaert D, Van Damme P, et al. T-cell receptor-induced JNK activation requires proteolytic inactivation of CYLD by MALT1. EMBO JOURNAL. 2011;30(9):1742–52.
MLA
Staal, Jens, Yasmine Driege, Tine Bekaert, et al. “T-cell Receptor-induced JNK Activation Requires Proteolytic Inactivation of CYLD by MALT1.” EMBO JOURNAL 30.9 (2011): 1742–1752. Print.
@article{1887628,
  abstract     = {The paracaspase mucosa-associated lymphoid tissue 1 (MALT1) is central to lymphocyte activation and lymphomagenesis. MALT1 mediates antigen receptor signalling to NF-kappa B by acting as a scaffold protein. Furthermore, MALT1 has proteolytic activity that contributes to optimal NF-kappa B activation by cleaving the NF-kappa B inhibitor A20. Whether MALT1 protease activity is involved in other signalling pathways, and the identity of the relevant substrates, is unknown. Here, we show that T-cell receptors (TCR) activation, as well as overexpression of the oncogenic API2-MALT1 fusion protein, results in proteolytic inactivation of CYLD by MALT1, which is specifically required for c-jun N-terminal kinase (JNK) activation and the inducible expression of a subset of genes. These results indicate a novel role for MALT1 proteolytic activity in TCR-induced JNK activation and reveal CYLD cleavage as the underlying mechanism.},
  author       = {Staal, Jens and Driege, Yasmine and Bekaert, Tine and Demeyer, Annelies and Muyllaert, David and Van Damme, Petra and Gevaert, Kris and Beyaert, Rudi},
  issn         = {0261-4189},
  journal      = {EMBO JOURNAL},
  keyword      = {signal transduction,ubiquitination,NF-KAPPA-B,UBIQUITIN-DEPENDENT KINASE,CYTOKINE PRODUCTION,DEUBIQUITINATING ENZYME CYLD,TUMOR-SUPPRESSOR CYLD,CARMA3/BCL10/MALT1 COMPLEX,SIGNALING PATHWAY,NEGATIVE REGULATION,TAK1,PROTEIN,MAP kinase,cytokine,AP-1},
  language     = {eng},
  number       = {9},
  pages        = {1742--1752},
  title        = {T-cell receptor-induced JNK activation requires proteolytic inactivation of CYLD by MALT1},
  url          = {http://dx.doi.org/10.1038/emboj.2011.85},
  volume       = {30},
  year         = {2011},
}

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