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:
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:
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:
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:
Proteins capable of modulating or mediating the function of MORT-1 are disclosed. Also disclosed are DNA sequences encoding these proteins, the recombinant production of these proteins as well as their use.
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.
Abstract translation:公开了肿瘤坏死因子受体(TNF-Rs)的抗体及其生产方法。 抗体优选是抑制TNF的细胞毒作用但不与TNF-R结合的抗体。 最优选地,抗体结合p75 TNF受体的C-末端半胱氨酸环的细胞外结构域,该环由SEQ ID NO:3的氨基酸序列Cys-185至Thr-201组成。
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:
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.