摘要:
The present invention relates to the three dimensional solution structure of the N-terminal domain of TNFR-1 associated death domain protein (“N-TRADD”), as well as the identification and characterization of a C-TRAF2 binding active site of N-TRADD. Also provided for by the present invention are methods of utilizing the three dimensional structures for the design and selection of potent and selective inhibitors of TNF signaling pathways.
摘要:
The present invention relates to the three dimensional solution structure of the N-terminal domain of TNFR-1 associated death domain protein (“N-TRADD”), as well as the identification and characterization of a C-TRAF2 binding active site of N-TRADD. Also provided for by the present invention are methods of utilizing the three dimensional structures for the design and selection of potent and selective inhibitors of TNF signaling pathways.
摘要:
The present invention relates to the three dimensional solution structure of receptor interacting protein dead domain (RIP DD), as well as the identification and characterization of various binding active sites of RIP DD. Also provided for by the present invention are methods of utilizing the three dimensional structure for the design and selection of potent and selective inhibitors of TNF signaling pathways.
摘要:
Polynucleotides encoding DADD protein are also disclosed, along with vectors, host cells, and methods of making DADD protein. Methods of identifying inhibitors of DADD death domain binding and inhibitors identified by such methods are also disclosed.
摘要:
Polynucleotides encoding DADD protein are also disclosed, along with vectors, host cells, and methods of making DADD protein. Methods of identifying inhibitors of DADD death domain binding and inhibitors identified by such methods are also disclosed.
摘要:
Polynucleotides encoding DADD protein are also disclosed, along with vectors, host cells, and methods of making DADD protein. Methods of identifying inhibitors of DADD death domain binding and inhibitors identified by such methods are also disclosed.
摘要:
Methods and compositions for modulating neural cell function using antagonists of TLR14 are disclosed. In particular, methods for treating, preventing and/or diagnosing TLR14-associated neurodegenerative conditions and/or disorders are disclosed. Screening methods for evaluating TLR14 modulators, e.g., agonists and antagonists, are also disclosed.
摘要:
The invention relates to compositions and methods comprising lymphotoxin-beta receptor (LTβR) modulators, which activate or inhibit LTβR signaling. LTβR modulators are useful for treating lymphocyte mediated immunological diseases and cancer, and more particularly, for regulating mitochondrial-mediated apoptosis. This invention relates to soluble forms of the LTβR complex proteins that act as LTβR activating or inhibiting agents. This invention also relates to the use of soluble molecules, directed against either the LTβR, its ligands, LIGHT and LTβ1α2, or its intracellular binding partners, that function to regulate LTβR signaling. A novel screening method for selecting soluble receptors, antibodies and other agents that modulate LTβR signaling is provided.
摘要:
Novel TNF receptor death domain ("TNF-R1-DD") ligand proteins are disclosed. Polynucleotides encoding the TNF-R1-DD ligand protein are also disclosed, along with vectors, host cells, and methods of making the TNF-R1-DD ligand protein. Pharmaceutical compositions containing the TNF-R1-DD ligand protein, methods of treating inflammatory conditions, and methods of inhibiting TNF-R death domain binding are also disclosed. Methods of identifying inhibitors of TNF-R death domain binding and inhibitors identified by such methods are also disclosed.
摘要:
Novel TNF receptor death domain (“TNF-R1-DD”) ligand proteins are disclosed. Polynucleotides encoding the TNF-R1-DD ligand protein are also disclosed, along with vectors, host cells, and methods of making the TNF-R1-DD ligand protein. Pharmaceutical compositions containing the TNF-R1-DD ligand protein, methods of treating inflammatory conditions, and methods of inhibiting TNF-R death domain binding are also disclosed. Methods of identifying inhibitors of TNF-R death domain binding and inhibitors identified by such methods are also disclosed.