Abstract: The present invention relates to in vitro and in vivo assays for the identification of agents that are useful in the treatment of neurodegenerative diseases that are associated with defects in protein folding. The present further relates to in vitro and in vivo assays for the identification of agents that contribute to the neurodegenerative processes which occur in these diseases. The present invention also relates to in vitro and in vivo models of neurodegenerative diseases. These assays and models will be useful in further understanding the pathogenesis of various neurodegenerative diseases in which defects in protein folding have been implicated, in identifying additional endogenous or environmental factors that contribute to the etiologies of these diseases, and in developing effective therapies for the prevention and/or treatment of these diseases.

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: The present invention is directed to novel polypeptides and to nucleic acid molecules encoding those polypeptides. Also provided herein are vectors and host cells comprising those nucleic acid sequences, chimeric polypeptide molecules comprising the polypeptides of the present invention fused to heterologous polypeptide sequences, antibodies which bind to the polypeptides of the present invention and to methods for producing the polypeptides of the present invention.

Abstract: The present invention provides a method for modifying the activity of NMDA (N-methyl-D-aspartate)receptors in cells by inhibition of the interaction of the unique domain of the tyrosine kinase Src enzyme and the NMDA receptor complex.

Abstract: The present invention is directed to novel polypeptides and to nucleic acid molecules encoding those polypeptides. Also provided herein are vectors and host cells comprising those nucleic acid sequences, chimeric polypeptide molecules comprising the polypeptides of the present invention fused to heterologous polypeptide sequences, antibodies which bind to the polypeptides of the present invention and to methods for producing the polypeptides of the present invention.

Abstract: This invention relates to a novel polypeptide involving in the modulation of central nervous system function, circulatory function, immune function, gastrointestinal function, metabolic function, reproductive function, etc., it can be used as a drug for treating or preventing a variety of diseases, e.g. HIV infection or AIDS (acquired immune deficiency syndrome) or the like.

Abstract: Targeted therapeutics that localize to a specific subcellular compartment such as the lysosome are provided. The targeted therapeutics include a therapeutic agent and a targeting moiety that binds a receptor on an exterior surface of the cell, permitting proper subcellular localization of the targeted therapeutic upon internalization of the receptor. Nucleic acids, cells, and methods relating to the practice of the invention are also provided.

Abstract: In methods for screening treatments for, and treatment of, neurodegenerative diseases, aggregation in neurons of NACP/?-synuclein is measured and expression of a non-amyloidogenic protein is stimulated in order to reduce the level aggregration. For purposes of screening agents for treatment of neurodegenerative disease, oxidative stress in the neuronal cells is stimulated by introducing a mixture of metal-ions and hydrogen peroxide. Examples of appropriate metals include iron, aluminum, and copper. After introduction of the agent under evaluation for stimulation of expression of non-amyloidogenic protein, the effectiveness is measured by testing for a decrease in the level of aggregation of NACP/?-synuclein. In an exemplary embodiment, the non-amyloidogenic protein is ?-synuclein. The aggregation of NACP/?-synuclein is dependent upon the concentration of metal ions in the neuronal cells.

Abstract: It has been discovered that dysferlin is expressed in blood and that individuals who lack dysferlin in muscle also lack it in CD14(+) cells. Based on these discoveries, blood-based tests for dysferlin expression and uses of such tests are described.

Abstract: A method of measuring the individual response to antidepressant drug therapy on the transport inhibition of monoamine neurotransmitters involves in vitro monitoring of radiolabeled monoamine neurotransmitter transport into cells transfected with transport proteins similar to those on neural cells of the individual being studied. The transport occurs in unbuffered serum of the individual who is undergoing or will later undergo pharmaceutical treatment for depression or other neuropsychiatric disorders. The use of buffers is avoided so that the sensitive balance of bound/free drug within the individuals serum is not disrupted prior to or during testing.

Abstract: The present invention relates generally to therapeutic methods and compositions. More particularly, methods and compositions to counteract and reverse disease-causing signaling defects in diseases with underlying signal transduction aberrations, including but not limited to Alzheimer's Disease.

Abstract: Human GABA transporter2 like protein polypeptides and polynucleotides and methods for producing such polypeptides by recombinant techniques are disclosed. Also disclosed are methods for utilizing human GABA transporter2 like protein polypeptides and polynucleotides in diagnostic assays.