Universiteit Gent

Vlaams Interuniversitair Instituut Voor Biotechnologie Vzw

Vib Vzw

Katholieke Universiteit Leuven, Ku Leuven R&d

Vrije Universiteit Brussel

Rudi Beyaert

Karen Heyninck

Walter C Fiers

Harald Braun

Frank Peelman

Bart Lambrecht

Peter Marynen

Kenneth Verstraete

Hamida Hammad

Savvas Savvides

Claude Libert

Hilde Revets

Thijs Baens

Lieven Huang

Sophie Janssens

Ben Wielockx

Sofie Van Huffel

Filip Delaei

Sigrid Cornelis

The present invention relates to monomeric fusion proteins comprising the extracellular part of the thymic stromal lymphopoietin receptor (TSLPR) and the extracellular part of the interleukin-7 receptor alpha (IL-7Ralpha) as inhibitors of thymic stromal lymphopoietin (TSLP) activity. The invention relates further to the use of said inhibitors as a medicament in the treatment of&#x2014;but not limited to&#x2014;inflammatory diseases, cancer and fibrosis.

TSLP inhibitors

The present invention relates to novel inhibitors of IL-33. More specifically, it relates to a fusion protein of the soluble IL-33 receptor with the soluble IL-1RAcP as inhibitor of IL-33 activity. The invention relates further to the use of the inhibitor in treatment of IL-33-related diseases such as, but not limited to, asthma, atopic dermatitis and psoriasis.

IL-33R and IL-1RAcP fusion proteins

The present invention relates to inhibitors of MALT1 proteolytic and/or autoproteolytic activity. More specifically, it relates to compounds such as, but not limited to peptide derivates such as Z-LSSR-CHO (see SEQ ID NO:1), Z-LSSR-CMK (see SEQ ID NO:1), Z-GASR-CHO (see SEQ ID NO:2), and Z-GASR-CMK (see SEQ ID NO:2), and small compounds such as 5-{[5-(3-chloro-4-methylphenyl)-2-furyl]methylene}-2-thioxodihydro-4,6(1H,5H)-pyrimidinedione and variants thereof, and the use of those compounds for the preparation of a medicament. The invention relates further to a method to screen for inhibitors of the MALT1 proteolytic and/or autoproteolytic activity.

Inhibitors of MALT1 proteolytic activity and uses thereof

The present invention relates to the treatment of epidermal growth factor-family receptor- (ErbB-) dependent tumors. More specifically, the present invention relates to the use of ABIN for the preparation of a medicament to inhibit epidermal growth factor- (EGF-) induced proliferation, and to treat ErbB-dependent tumors.

Treatment of EGFR-dependent tumors by ABIN (a20 -binding inhibitor of NF kappab)

The present invention relates to novel inhibitors of the Nuclear factor kappa B (NF-&#x3ba;B) activating pathway useful in the treatment of NF-&#x3ba;B related diseases and/or in the improvement of anti-tumor treatments. These inhibitors interfere early in the TRAF induced signaling pathway and are therefore more specific than I&#x3ba;B.

Inhibitors of NF-kappaB activation

The present invention relates to the field of infection and inflammation and, more specifically, to the field of pathogen-induced nuclear factor kappa B activation. More specifically, a novel splice variant of MyD88, (MyD88), which has been identified encoding a protein that inhibits LPS-induced NF-&#x3ba;B activation. MyD88is a target to inhibit the phenomenon of endotoxin-tolerance that occurs in sepsis.

Splice variant of MyD88 and uses thereof

The present invention relates to the use of the A20-binding inhibitor of NF-&#x3ba;B activation (ABIN), or a functional fragment or variant thereof to protect against TNF-induced liver failure, such as viral hepatitis and alcoholic liver disease. More particularly, it relates to the prevention of the toxic effects of said diseases, including lethality, by overexpressing ABIN.

Abin-mediated hepatitis protection

Two isoforms, p110 and p58 of PITSLRE protein kinase, can be translated from the same p110 (a2-2) mRNA by an internal ribosome entry process. Accordingly, p110 and p58, two proteins with punitive functions, are translated from a single mRNA species by using two AUGs within the same reading frame. These two proteins share the 439 C-terminal amino acids that contain the kinase domain. The internal ribosomal entry site (&ldquo;IRES&rdquo;) in the polycistronic p110 mRNA is the first IRES completely localized in the coding region of a cellular mRNA. Moreover, it was unexpectedly found that the IRES element is cell cycle regulated. Translation of p58 occurs in the G2/M stage of the cycle.

Internal ribosome entry site, vector containing same and uses thereof

The present invention relates to novel inhibitors of the Nuclear factor kappa B (NF-&kgr;B) activating pathway useful in the treatment of NF-&kgr;B related diseases and/or in the improvement of anti-tumor treatments. These inhibitors interfere early in the TRAF induced signaling pathway and are therefore more specific than I&kgr;B.

Growing community of inventors

Zingem, Belgium

Rudi Beyaert