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Regulation of NF-κB signaling by caspases and MALT1 paracaspase

Jens Staal UGent, Tine Bekaert UGent and Rudi Beyaert UGent (2011) CELL RESEARCH. 21(1). p.40-54
abstract
Caspases are intracellular proteases that are best known for their function in apoptosis signaling. It has become evident that many caspases also function in other signaling pathways that propagate cell proliferation and inflammation, but studies on the inflammatory function of caspases have mainly been limited to caspase-1-mediated cytokine processing. Emerging evidence, however, indicates an important contribution of caspases as mediators or regulators of nuclear factor-kappa B (NF-kappa B) signaling, which plays a key role in inflammation and immunity. Much still needs to be learned about the mechanisms that govern the activation and regulation of NF-kappa B by caspases, and this review provides an update of this area. Whereas apoptosis signaling is dependent on the catalytic activity of caspases, they mainly act as scaffolding platforms for other signaling proteins in the case of NF-kappa B signaling. Caspase proteolytic activity, however, counteracts the pro-survival function of NF-kappa B by cleaving specific signaling molecules. A striking exception is the paracaspase mucosa-associated lymphoid tissue 1 (MALT1), whose adaptor and proteolytic activity are both needed to initiate a full blown NF-kappa B response in antigen-stimulated lymphocytes. Understanding the role of caspases and MALT1 in the regulation of NF-kappa B signaling is of high interest for therapeutic immunomodulation.
Please use this url to cite or link to this publication:
author
organization
alternative title
Regulation of NF-kappa B signaling by caspases and MALT1 paracaspase
year
type
journalArticle (review)
publication status
published
subject
keyword
paracaspase, caspases, NF-kappa B, MALT1, TNF, inflammation, apoptosis, T-CELL-ACTIVATION, NUCLEAR-FACTOR, IKK-ALPHA, CYTOKINE PRODUCTION, ANTIGEN RECEPTOR, DNA-DAMAGE, CARMA3/BCL10/MALT1 COMPLEX, MEDIATED CLEAVAGE, TUMOR SUPPRESSION, INDUCED APOPTOSIS
journal title
CELL RESEARCH
Cell Res.
volume
21
issue
1
pages
40 - 54
Web of Science type
Review
Web of Science id
000285867600005
JCR category
CELL BIOLOGY
JCR impact factor
8.19 (2011)
JCR rank
23/178 (2011)
JCR quartile
1 (2011)
ISSN
1001-0602
DOI
10.1038/cr.2010.168
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
2003563
handle
http://hdl.handle.net/1854/LU-2003563
date created
2012-01-25 17:35:15
date last changed
2013-02-27 09:09:27
@article{2003563,
  abstract     = {Caspases are intracellular proteases that are best known for their function in apoptosis signaling. It has become evident that many caspases also function in other signaling pathways that propagate cell proliferation and inflammation, but studies on the inflammatory function of caspases have mainly been limited to caspase-1-mediated cytokine processing. Emerging evidence, however, indicates an important contribution of caspases as mediators or regulators of nuclear factor-kappa B (NF-kappa B) signaling, which plays a key role in inflammation and immunity. Much still needs to be learned about the mechanisms that govern the activation and regulation of NF-kappa B by caspases, and this review provides an update of this area. Whereas apoptosis signaling is dependent on the catalytic activity of caspases, they mainly act as scaffolding platforms for other signaling proteins in the case of NF-kappa B signaling. Caspase proteolytic activity, however, counteracts the pro-survival function of NF-kappa B by cleaving specific signaling molecules. A striking exception is the paracaspase mucosa-associated lymphoid tissue 1 (MALT1), whose adaptor and proteolytic activity are both needed to initiate a full blown NF-kappa B response in antigen-stimulated lymphocytes. Understanding the role of caspases and MALT1 in the regulation of NF-kappa B signaling is of high interest for therapeutic immunomodulation.},
  author       = {Staal, Jens and Bekaert, Tine and Beyaert, Rudi},
  issn         = {1001-0602},
  journal      = {CELL RESEARCH},
  keyword      = {paracaspase,caspases,NF-kappa B,MALT1,TNF,inflammation,apoptosis,T-CELL-ACTIVATION,NUCLEAR-FACTOR,IKK-ALPHA,CYTOKINE PRODUCTION,ANTIGEN RECEPTOR,DNA-DAMAGE,CARMA3/BCL10/MALT1 COMPLEX,MEDIATED CLEAVAGE,TUMOR SUPPRESSION,INDUCED APOPTOSIS},
  language     = {eng},
  number       = {1},
  pages        = {40--54},
  title        = {Regulation of NF-\ensuremath{\kappa}B signaling by caspases and MALT1 paracaspase},
  url          = {http://dx.doi.org/10.1038/cr.2010.168},
  volume       = {21},
  year         = {2011},
}

Chicago
Staal, Jens, Tine Bekaert, and Rudi Beyaert. 2011. “Regulation of NF-κB Signaling by Caspases and MALT1 Paracaspase.” Cell Research 21 (1): 40–54.
APA
Staal, J., Bekaert, T., & Beyaert, R. (2011). Regulation of NF-κB signaling by caspases and MALT1 paracaspase. CELL RESEARCH, 21(1), 40–54.
Vancouver
1.
Staal J, Bekaert T, Beyaert R. Regulation of NF-κB signaling by caspases and MALT1 paracaspase. CELL RESEARCH. 2011;21(1):40–54.
MLA
Staal, Jens, Tine Bekaert, and Rudi Beyaert. “Regulation of NF-κB Signaling by Caspases and MALT1 Paracaspase.” CELL RESEARCH 21.1 (2011): 40–54. Print.