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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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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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MLA
Staal, Jens, et al. “T-Cell Receptor-Induced JNK Activation Requires Proteolytic Inactivation of CYLD by MALT1.” EMBO JOURNAL, vol. 30, no. 9, 2011, pp. 1742–52, doi:10.1038/emboj.2011.85.
APA
Staal, J., Driege, Y., Bekaert, T., Demeyer, A., Muyllaert, D., Van Damme, P., … Beyaert, R. (2011). T-cell receptor-induced JNK activation requires proteolytic inactivation of CYLD by MALT1. EMBO JOURNAL, 30(9), 1742–1752. https://doi.org/10.1038/emboj.2011.85
Chicago author-date
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): 1742–52. https://doi.org/10.1038/emboj.2011.85.
Chicago author-date (all authors)
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. doi:10.1038/emboj.2011.85.
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.
IEEE
[1]
J. Staal et al., “T-cell receptor-induced JNK activation requires proteolytic inactivation of CYLD by MALT1,” EMBO JOURNAL, vol. 30, no. 9, pp. 1742–1752, 2011.
@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}},
  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}},
  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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