Abstract: Proteins capable of modulating the function of FAS/APO1 are provided. The proteins may be prepared by culturing a host cell transformed with a vector containing the DNA encoding such a protein under suitable conditions and isolating the protein.

Abstract: Antibodies to tumor necrosis factor receptors (TNF-Rs) are disclosed together with methods of producing them and methods of use of such antibodies in immunoassays and purification of TBP-II by affinity chromatography. A diagnostic assay for endogenous antibodies to TBP-II is also disclosed.

Abstract: There are provided proteins which interact with caspase-8. Production and use of such proteins is also provided.

Abstract: A protein capable of modulating or mediating the intracellular activity of RIP in inflammation, cell survival and cell death pathways is provided. DNA encoding it, a method for its production and its uses are also provided.

Abstract: The present invention generally concerns novel proteins which bind to the intracellular domains of the p55 and p75 TNF-Rs and the FAS-R, which are capable of modulating the function of the p55 and p75 TNF-Rs and the FAS-R, and the DNA sequences which encode them. The present invention also concerns new soluble oligomeric TNF-Rs, oligomeric FAS-Rs and oligomeric receptors having a mixture of TNF-Rs and FAS-Rs. In addition, the present invention concerns methods of preparation and uses of all of the aforementioned.

Abstract: Antibodies to Tumor Necrosis Factor receptors (TNF-Rs) which inhibit the cytocidal effect of TNF but not its binding to the TNF-Rs, and ligands interacting with other receptors of the TNF/NGF family, are provided together with methods of producing them. The antibodies preferably bind to the fourth cysteine rich domain of the p75 TNF receptor or to the region between said fourth cysteine rich domain and the cell membrane.

Abstract: The present invention provides proteins capable of modulating or mediating the FAS receptor ligand or TNF effect on cells carrying FAS receptor or p55 receptor by binding or interacting with MORT-1 protein, which in turn binds to the intracellular domain of the FAS receptor or to another protein TRADD which binds to the p55 receptor. In addition, peptide inhibitors that interfere with the proteolytic activity of MORT-1-binding proteins having proteolytic activity are provided, as well as a method of designing them.

Abstract: DNA encoding Antibodies to tumor necrosis factor receptors (TNF-Rs) are disclosed. The antibodies are preferably those which inhibit the cytotoxic effect of TNF but not its binding to the TNF-Rs. Most preferably, the antibodies bind to an extracellular domain of the C-terminal cysteine loop of the p75 TNF receptor, which loop consists of the amino acid sequence Cys-185 to Thr-201 of SEQ ID NO:3.

Abstract: Tumor Necrosis Factor (TNF) Binding Protein is isolated and substantially purified. It has the ability to inhibit the cytotoxic effect of TNF and/or to maintain its prolonged beneficial effects. Isolated cDNA encoding TNF Binding Protein II is obtained and may be used to produce expression vectors, prokaryotic or eukaryotic expression hosts and methods of obtaining the protein by culturing of such hosts.

Abstract: The present invention provides proteins capable of modulating or mediating the FAS receptor ligand or TNF effect on cells carrying FAS receptor or p55 receptor by binding or interacting with MORT-1 protein, which in turn binds to the intracellular domain of the FAS receptor or to another protein TRADD which binds to the p55 receptor. In addition, peptide inhibitors which interfere with the proteolytic activity of MORT-1-biding proteins having proteolytic activity are provided as well as a method of designing them.

Abstract: The present invention generally concerns novel proteins which bind to the intracellular domains of the p55 and p75 TNF-Rs and the FAS-R, which are capable of modulating the function of the p55 and p75 TNF-Rs and the FAS-R, and the DNA sequences which encode them. The present invention also concerns new soluble oligomeric TNF-Rs, oligomeric FAS-Rs and oligomeric receptors having a mixture of TNF-Rs and FAS-Rs. In addition, the present invention concerns methods of preparation and uses of all of the aforementioned.

Abstract: Antibodies to Tumor Necrosis Factor receptors (TNF-Rs) which inhibit the cytocidal effect of TNF but not its binding to the TNF-Rs, and ligands interacting with other receptors of the TNF/NGF family, are provided together with methods of producing them. The antibodies preferably bind to the fourth cysteine rich domain of the p75 TNF receptor or to the region between said fourth cysteine rich domain and the cell membrane.

Abstract: Proteins which are capable of modulating/mediating the function of RIP, their preparation and uses are provided.

Abstract: A promoter sequence of the human p55 TNF-R gene is provided. Also provided are sequence motifs and motif regions contained within the promoter sequence. Methods for preparing these motifs or motif regions and their use in the modulation of TNF function are also provided.

Abstract: Tumor Necrosis Factor (TNF) Inhibitory Protein is isolated and substantially purified. It has the ability to inhibit: (a) the binding of TNF to its receptors, and (b) the cytotoxic effect of TNF. TNF Inhibitory Protein and salts, functional derivatives and active fractions thereof can be used to antagonize the deleterious effects of TNF.

Abstract: Recombinant DNA encoding Tumor Necrosis Factor (TNF) Inhibitory Protein, or an active fragment thereof, is obtained. The TNF Inhibitory Protein has the ability to inhibit: (a) the binding of TNF to its receptors, and (b) the cytotoxic effect of TNF. TNF Inhibitory Protein and salts, functional derivatives and active fractions thereof can be used to antagonize the deleterious effects of TNF by eliminating TNF from the body, and to reduce the cytotoxic activity of TNF by binding to TNF and thereby to inhibit the binding of TNF to its receptors. The DNA may be in an expression vector. Host cells transfected with such an expression vector may be used to produce the TNF Inhibitory Protein.

Abstract: Tumor Necrosis Factor (TNF) Inhibitory Protein is isolated and substantially purified. It has the ability to inhibit: (a) the binding of TNF to its receptors, and (b) the cytotoxic effect of TNF. TNF Inhibitory Protein and salts, functional derivatives and active fractions thereof can be used to antagonize the deleterious effects of TNF by eliminating TNF from the body, and to reduce the cytotoxic activity of TNF by binding to TNF and thereby to inhibit the binding of TNF to its receptors.

Abstract: A method of modulating signal transduction and/or cleavage in Tumor Necrosis Factor Receptors (TNF-Rs) is provided. Peptides or other molecules may interact either with the receptor itself, or with effector proteins interacting with the receptor, thus modulating the normal functioning of the TNF-Rs. Such peptides or other molecules may be employed for prophylactic and therapeutic applications in TNF associated diseases.

Abstract: A modulator of regulatory cellular events occurring intracellularly which are mediated by regulatory proteins containing a ‘death domain’ motif is provided. The ‘death domain’ is a regulatory portion of the regulatory proteins, and the modulator is capable of interacting with one or more ‘death domain’ motifs contained in the regulatory proteins and affecting the regulatory action of one or more of the regulatory proteins. The modulator preferably is capable of interacting with ‘death domain’ motifs within p55-TNF-R, FAS/APO1-R, NGF-R, MORT-1, RIP, TRADD, or ankyrin. A method for producing the modulators is also provided. The modulators are useful for modulating functions mediated in cells by proteins containing the ‘death domain’.

Abstract: Antibodies to tumor necrosis factor receptors (TNF-Rs) are disclosed together with methods of producing them. The antibodies are preferably those which inhibit the cytotoxic effect of TNF but not its binding to the TNF-Rs. Most preferably, the antibodies bind to an extracellular domain of the C-terminal cysteine loop of the p75 TNF receptor, which loop consists of the amino acid sequence Cys-185 to Thr-201 of SEQ ID NO:3.