Rudi Beyaert Lab

Research focus

The goal of our research is to understand the molecular mechanisms that control inflammation and immunity. We mainly focus on the nuclear factor-kappaB (NF-kB) signaling pathway, which is activated in response to injury, infection, inflammation and other stressful conditions requiring rapid reprogramming of gene expression. Inappropriate NF-kB dependent gene expression is implicated in the pathogenesis of inflammatory diseases and cancer. We are using several molecular and biochemical approaches to generate fundamental knowledge on the biology of a limited subset of molecules that control NF-κB signaling downstream of key cytokine (e.g. TNF, IL-1, IL-33) and immune receptors (e.g. TLR, TCR). The pathophysiological role of our in vitro findings is validated in appropriate disease models (e.g. multiple sclerosis, rheumatoid arthritis, Crohn’s disease, Influenza infection, inflammation associated cancer).

Specific research topics include:

  1. Regulation of NF-kB and IRF signaling by ubiquitin binding proteins;
  2. Molecular regulation of the ubiquitin-editing protein A20;
  3. Study of the pathophysiological role of A20 using tissue-specific gene targeting and mouse models of disease; (see research focus Geert van Loo)
  4. Biological function, regulation, and novel substrates of paracaspase MALT1;
  5. Cross-talk between TCR and glutamate receptor signaling;
  6. ER stress and NF-κB signaling
  7. NF-κB signaling and selective autophagy.


SUBGROUP GEERT VAN LOO
(Lars Vereecke, Conor McGuire, Leen Catrysse, Mozes Sze, Stefano Bonelli)

Bio
PhD: Univ. of Ghent, Ghent, Belgium, 2002
Post-doc: EMBL, Monterotondo, Italy, 2002-2005
Staff scientist at VIB, Ghent, Belgium since 2007
Professor at Ghent University, Ghent, Belgium since 2011

Contact Info
VIB Department for Molecular Biomedical Research – UGent
VIB Research Building FSVM
Technologiepark 927 9052 GENT
Geert.vanloo*Replace*With*At*Sign*dmbr.vib-UGent.be
Phone: +32 9 331 37 62     

Research focus
Research in this subgroup, headed by Geert van Loo, focusses on the in vivo mechanisms by which inflammation drives (autoimmune) pathology. For these studies, they make use of Cre/LoxP-mediated gene targeting technology, allowing tissue-specific gene deletion in mice, in combination with mouse models of human inflammatory disease. Central in their research is the study of the molecular mechanisms involving NF-kB, apoptosis and ER stress in pathologies such as inflammatory bowel disease, rheumatoid arthritis, diabetes and multiple sclerosis.
 
Matmati M, Jacques P, Maelfait J, Verheugen E, Kool M, Sze M, Geboes L, Louagie E, Guire C, Vereecke L, Chu Y, Boon L, Staelens S, Matthys P, Lambrecht B, Schmidt-Supprian M, Pasparakis M, Elewaut D, Beyaert R, van Loo G
NATURE GENETICS, 43, 908-12, 2011
 
Welz PS, Wullaert A, Vlantis K, Kondylis E, Fernandez-Majada V, Ermolaeva M, Kirsch P, Sterner-Kock A, van Loo G, Pasparakis M
NATURE, 477, 330-334, 2011
 
Lippens S, Lefebvre S, Gilbert B, Sze M, Devos M, Verhelst K, Vereecke L, Mc Guire C, Guérin C, Vandenabeele P, Pasparakis M, Mikkola ML, Beyaert R, Declercq W, van Loo G
CELL DEATH DIFFER, 18, 1845-1853, 2011
 
Vereecke L, Sze M, McGuire C, Rogiers B, Chu Y, Schmidt-Supprian M, Pasparakis M, Beyaert R, van Loo G
JOURNAL OF EXPERIMENTAL MEDICINE, 207, 1513-23, 2010
 

Publications

A20 (Tnfaip3) Deficiency in Myeloid Cells Protects against Influenza A Virus InfectionMaelfait J, Roose K, Bogaert P, Sze M, Saelens X, Pasparakis M, Carpentier I, van Loo G, Beyaert RPLoS Pathogens, 8, e1002570, 2012
A20 (TNFAIP3) deficiency in myeloid cells triggers erosive polyarthritis resembling rheumatoid arthritisMatmati M, Jacques P, Maelfait J, Verheugen E, Kool M, Sze M, Geboes L, Louagie E, Guire C, Vereecke L, Chu Y, Boon L, Staelens S, Matthys P, Lambrecht B, Schmidt-Supprian M, Pasparakis M, Elewaut D, Beyaert R, van Loo GNATURE GENETICS, 43, 908-12, 2011
T-cell receptor-induced JNK activation requires proteolytic inactivation of CYLD by MALT1Staal J, Driege Y, Bekaert T, Demeyer A, Muyllaert D, Van Damme P, Gevaert K, Beyaert REMBO JOURNAL, 30, 1742-52, 2011
Enterocyte-specific A20 deficiency sensitizes to tumor necrosis factor-induced toxicity and experimental colitisVereecke L, Sze M, McGuire C, Rogiers B, Chu Y, Schmidt-Supprian M, Pasparakis M, Beyaert R, van Loo GJOURNAL OF EXPERIMENTAL MEDICINE, 207, 1513-23, 2010
T cell antigen receptor stimulation induces MALT1 paracaspase-mediated cleavage of the NF-kappaB inhibitor A20Coornaert B, Baens M, Heyninck K, Bekaert T, Haegman M, Staal J, Sun L, Chen Z, Marynen P, Beyaert RNATURE IMMUNOLOGY, 9, 263-71, 2008

News

Defect in A20 gene expression causes rheumatoid arthritis

16/08/2011 - In Nature Genetics, VIB-UGent researchers demonstrate that a defect in the expression of the A20 gene can contribute to the development of rheumatoid arthritis in mice, identifying A20 as a target for the generation of new drugs.

First step to new therapy for chronic bowel disease

05/07/2010 - Scientists associated with VIB and Ghent University (UGent) have discovered that A20 protein plays an important protective role in diseases associated with chronic bowel inflammation.

A major step toward a more targeted treatment for auto-immune diseases?

28/01/2008 - VIB researchers have elucidated the function of MALT1, a key player in controlling inflammatory reactions. They are the first to show that MALT1 is able to cleave the A20 protein, which inhibits inflammation.

Rudi Beyaert

Rudi Beyaert

Research area(s)

Model organism(s)

Bio

PhD: Univ. of Ghent, Ghent, Belgium, 1992
VIB Group leader since 1997
Full Professor at Ghent University, Ghent, Belgium since 2003
Associate Department Director since 2009

Contact Info

VIB Department for Molecular Biomedical ResearchUGentVIB Research Building FSVMTechnologiepark 927 9052 GENTRoute description