Abstract: The invention relates to compounds, in particular siRNAs, which inhibit the expression of specific human genes. The invention also relates to pharmaceutical compositions comprising such compounds and a pharmaceutically acceptable carrier. The present invention also provides a method of treating and/or preventing the incidence or severity of various diseases or conditions associated with the genes and/or symptoms associated with such diseases or conditions comprising administering to a subject in need of treatment for such disease or condition and/or symptom the compound or the pharmaceutical composition in a therapeutically effective dose so as to thereby treat the subject. The invention also provides antibodies which inhibit specified human polypeptides and pharmaceutical compositions comprising one or more such antibodies.

Abstract: A DNA sequence encoding a protein capable of binding to a tumor necrosis factor receptor-associated factor (TRAF) molecule, TRAF-binding proteins, their isoforms, analogs, fragments and derivatives encoded by the DNA sequence, their methods for the production of the DNA sequences and proteins, and the uses for the DNA sequence and proteins.

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 provides compositions and methods for alleviation or reduction of the symptoms and signs associated with damaged neuronal tissues whether resulting from tissue trauma, or from chronic or acute degenerative changes. In particular, some embodiments of the present invention provide one or more pharmaceutical compositions comprising as an active ingredient a BMP2A inhibitor further comprising a pharmaceutically acceptable diluent or carrier. An additional embodiment provides a method for reducing damage to the central nervous system in a patient who has suffered an injury to the central nervous system, comprising administering to the patient a pharmaceutical composition in a dosage sufficient to reduce the damage. Yet another embodiment provides of the use of a BMP2A inhibitor for the preparation of a medicament for promoting or enhancing recovery in a patient who has suffered an injury to the central nervous system.

Abstract: The present invention provides novel molecules, compositions, methods and uses for treating microvascular disorders, eye diseases respiratory conditions and hearing disorders based upon inhibition of the RTP801L gene and/or protein.

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: RTP801L represents a unique gene target for hypoxia-inducible factor-1 (HIF-1) that may regulate hypoxia-induced pathogenesis; down-regulation of the mTOR pathway activity by hypoxia requires de novo mRNA synthesis and correlates with increased expression of RTP801L. The present invention relates to screening systems utilizing RTP801L and/or RTP801L interactors and/or RTP801L biological activity, and to the potential drugs and methods of treatment identified by such screening systems.

Abstract: RTP801 represents a unique gene target for hypoxia-inducible factor-1 (HIF-1). Down-regulation of the mTOR pathway activity by hypoxia requires de novo mRNA synthesis and correlates with increased expression of RTP801. The present invention relates to screening systems utilizing RTP801 and/or RTP801 interactors and/or RTP801 biological activity, to drug candidates identified by such screening systems, and to the use of such drug candidates in the treatment of various disorders.

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: 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: The present invention relates to the field of diagnosis and treatment of neurodegenerative diseases, ischemic events, and central nervous system injury, and provides compositions and methods for alleviation or reduction of the symptoms and signs associated with damaged neuronal tissues whether resulting from tissue trauma, or from chronic or acute degenerative changes. The present invention in particular relates to the discovery that the expression of Annexin II is involved in apoptosis induced by oxidative stress, and that anti-sense Annexin II RNA and Annexin II siRNA protected the cells from this apoptosis. Thus Annexin II inhibitors prevent the damage caused by said ischemic event.

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: 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: 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: 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: Genes and the proteins encoded thereby that are involved in stroke response and/or are regulated by FK506 are disclosed. These genes were discovered using in vivo or in vitro stroke models by determining which genes were differentially upregulated or downregulated upon treatment of the model with FK506. They were also found by a functional assay of genes specifically selected for conferring to cells resistance to hypoxia, dopamine or glutamate treatment. The disclosure includes such genes and proteins as well as analogs, salts and functional derivatives of such proteins, and DNA encoding such analogs, and methods of use. Methods for treating the effects of stroke, hypoxia and/or ischemia by regulating such genes or proteins are disclosed. Methods for screening for compounds capable of regulating the genes and proteins of the invention are also disclosed.

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.

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.