Ghent University Academic Bibliography

Advanced

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
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.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
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
journal title
EMBO JOURNAL
Embo J.
volume
30
issue
9
pages
1742 - 1752
Web of Science type
Article
Web of Science id
000290307500008
JCR category
BIOCHEMISTRY & MOLECULAR BIOLOGY
JCR impact factor
9.205 (2011)
JCR rank
21/286 (2011)
JCR quartile
1 (2011)
ISSN
0261-4189
DOI
10.1038/emboj.2011.85
project
Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1887628
handle
http://hdl.handle.net/1854/LU-1887628
date created
2011-08-11 12:15:11
date last changed
2013-02-27 09:09:11
@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},
}

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.