Abstract: Methods of activating a signaling cascade comprising, introducing leptin and/or a cytokine to a receptor complex comprising gp 130, optionally in combination with a compound acting on adenylate cyclase or acting on one or more downstream targets of adenylate cyclase, thereby inducing genes in neuro-endocrine cells or cells of neuro-endocrine origin. Two distinct gene-sets are induced, immediate early response genes (STAT-3, SOCS-3, Metallothionein-II, the serine/threonine kinase Fnk and the rat homologue of MRF-1), and late induced target genes (Pancreatitis Associated Protein I, Squalene Epoxidase, Uridinediphosphate Glucuronyl Transferase and Annexin VIII). Strong co-stimulation with the adenylate cyclase activator forskolin was shown with respect to late induced target genes. Transcripts encoding Leptin Induced Protein I (LIP-I) and Leptin Induced Protein II (LIP-II) were identified; however, no forskolin co-stimulatory effect was observed.

Abstract: The invention provides reagents and methods for the accurate quantification of proteins in complex biological samples. Quantification is obtained by adding to a sample a peptide combo, which is essentially a collection of synthetic reference peptides. The synthetic reference peptides have a small mass difference when compared to the biological reference peptides that originate upon digestion from the proteins present in the sample. Reference peptides and synthetic reference peptides are selected and the identity and accurate amounts of reference peptides are determined by mass spectrometry. The methods can be used in high throughput assays to interrogate proteomes.

Abstract: The invention relates to adenoviral vectors. More particularly, this invention relates to recombinant high capacity adenoviral vectors which can be employed in the treatment of hemophilia A, as well as methods and process for their creation and use.

Abstract: The present invention relates to a functional fragment of a receptor having a function in signaling. Particularly, the present invention relates to a functional fragment of the leptin receptor, involved in SOCS3, CIS and/or Vav signaling.

Abstract: The present invention relates to neurological and physiological dysfunction associated with neuron disorders. In (particular, the invention relates to the involvement of vascular endothelial growth factor (VEGF) and homologues in the aetiology of motor neuron disorders. The invention further concerns a novel, mutant transgenic mouse (VEGFm/m) with a homozygous deletion in the hypoxia responsive element (HRE) of the VEGF promoter which alters the hypoxic upregulation of VEGF. These mice suffer severe adult onset muscle weakness due to progressive spinal motor neuron degeneration which is reminiscent of amyotrophic lateral sclerosis (ALS)—a fatal disorder with unknown aetiology. Furthermore, the neuropathy of these mice is not caused by vascular defects, but is due to defective VEGF-mediated survival signals to motor neurons.

Abstract: The present invention relates to a microorganism, preferably a bacterial strain, preferably a non-pathogenic strain, preferably a non-invasive strain, preferably a food grade strain, preferably a gram-positive bacterial strain, delivering a trefoil peptide in vivo. Preferably said trefoil peptide is TFF1. The present invention further relates to a method for the delivery of trefoil peptide to the gastro-intestinal tract comprising the administration of such a bacterial strain. The present invention also relates to a pharmaceutical composition comprising a trefoil peptide delivering bacterium as well as methods of treatment of acute gastro-intestinal inflammatory diseases comprising administration of said transformed bacterial strains, particularly for treating acute colitis, including but not limited to acute flare-ups of Crohn's disease and ulcerative colitis in humans, as well as for treating gastro-intestinal disorders of a similar nature in other animal species.

Abstract: The present invention relates generally to the field of human genetics. Specifically, the present invention relates to methods and materials used to diagnose distal hereditary motor neuropathy type II by detecting polymorphisms in HSP22 gene.

Abstract: The present invention relates to the identification of the molecular binding domains between presenilins and its substrates such as amyloid precursor protein and telencephalin. These binding domains can be efficiently used in drug screening assays to screen for compounds capable of modulating the interaction between presenilins and type I transmembrane proteins. The invention further relates to compounds capable of modulating the interaction.

Abstract: The present invention relates to a phosphorylated form of mammalian glyoxalase I. The present invention relates further to the use of phosphorylated mammalian glyoxalase I to modulate MG-modification of proteins (AGE formation) and consequent cell death, especially upon stress such as oxidative stress, or upon TNF treatment.

Abstract: Described is a method of modulating E-cadherin mediated cell adhesion. More specifically, described is the use of hECRep1a and homologues thereof to modulate and/or control tumor cell invasiveness.

Abstract: The present invention relates to a phosphorylated form of mammalian glyoxalase I. The present invention relates further to the use of phosphorylated mammalian glyoxalase I to modulate MG-modification of proteins (AGE formation) and consequent cell death, especially upon stress such as oxidative stress, or upon TNF treatment.

Abstract: The present invention relates to a method for cloning immunoglobulin variable domain sequences derived from immunoglobulins, and a repertory library of immunoglobulin variable domain sequences made according to the method.

Abstract: The present invention relates to an influenza antigen, comprising a fusion product of at least the extracellular part of a conserved influenza membrane protein or a functional fragment thereof and a presenting carrier, which may be a presenting (poly)peptide or a non-peptidic structure, such as glycans, peptide mimetics, synthetic polymers. The invention further relates to a vaccine against influenza, comprising at least an antigen of the invention, optionally in the presence of one or more excipients. The invention also relates to use of the antigen, a method for preparing the antigen and acceptor cells expressing the antigen.

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: Described are methods of modulating stem/progenitor cell recruitment involving molecules that agonize the formation of plasmin stimulating the recruitment of stem/progenitor cells, including hematopoietic and endothelial precursor cells. Conversely, antagonists of plasmin can inhibit recruitment of the stem cells. In addition, the identification of the uPA receptor (uPAR) as a retention signal for stem cells in their niche suggests a novel method for increased engraftment and isolation of multipotent stem cells.

Abstract: The present invention relates to novel proteins interacting with the cytoplasmic domain of CD40, which are useful in the treatment of CD40 and/or NF-?B related diseases. Surprisingly, these proteins do not show significant amino acid sequence identity with the members of tumor necrosis factor receptor associated factor (TRAF) family; and thus, offer the possibility to modulate the CD40 and/or NF-?B signaling pathway independently from interaction of TRAF with CD40.

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 novel markers for alternatively activated macrophages. More specifically, the present invention relates to the use of galactose-type C-type lectins as surface markers that allows rapid identification and sorting of the alternative macrophages. Such identifications can be useful in diseases where there is an imbalance between proinflammatory and anti-inflammatory immune reactions.

Abstract: The present invention relates to L-gulose dependent vitamin C synthesis. More specifically, the present invention relates to a synthesis pathway of vitamin C, comprising the formation of GDP-L-gulose by GDP-mannose 3?,5?-epimerase, and subsequent transformation into L-gulose and L-ascorbic acid.

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.