Abstract: 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—but not limited to—inflammatory diseases, cancer and fibrosis.

Abstract: 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.

Abstract: 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—but not limited to—inflammatory diseases, cancer and fibrosis.

Abstract: 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.

Abstract: 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.

Abstract: 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.

Abstract: 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.

Abstract: 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.

Abstract: The present invention relates to novel inhibitors of the Nuclear factor kappa B (NF-?B) activating pathway useful in the treatment of NF-?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?B.

Abstract: 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, (MyD88S), which has been identified encoding a protein that inhibits LPS-induced NF-?B activation. MyD88S is a target to inhibit the phenomenon of endotoxin-tolerance that occurs in sepsis.

Abstract: The present invention relates to the use of the A20-binding inhibitor of NF-?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.

Abstract: The present invention relates to ubiquitinated TNF receptor 2, and the uses thereof. More specifically, the invention relates to the use of TNF receptor 2 ubiquitination to deplete TNF receptor 2 from the cell membrane and cytoplasm, and relocalize it in the insoluble cell fraction. Such relocalization can be used to modulate the signaling activity of the TNF receptor 2 and to treat TNF receptor 2-related diseases. The invention relates further to the use of Smurf 2 to ubiquitinate TNF receptor 2 and to the use of TRAF2 to mediate TNF receptor 2 ubiquitination.

Abstract: The present invention relates to the use of Yops as caspase inhibitors. More specifically, it relates to the use of YopE and YopT as inhibitors of caspase-1 activity. The inhibitor can be used to treat caspase-1-related pathologies, such as inflammatory diseases and to inhibit caspase-1-related and/or -mediated cell death.

Abstract: 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, (MyD88S), which has been identified encoding a protein that inhibits LPS-induced NF-?B activation. MyD88S is a target to inhibit the phenomenon of endotoxin-tolerance that occurs in sepsis.

Abstract: 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 (“IRES”) 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.

Abstract: The present invention relates to the use of the A20-binding inhibitor of NF-&kgr;B activation (ABIN), or a functional fragment or variant thereof to protect aGalNst 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.

Abstract: 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.

Abstract: 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.

Abstract: 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 putative different 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 (“IRES”) 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 cell cycle.