The invention provides isolated N-methyl-D-aspartate type 3B (NR3B) polypeptides, functional fragments and peptides, encoding nucleic acid molecules and polynucleotides, and specific antibodies. Also provided are excitatory glycine receptors, containing either NR3B or NR3A polypeptides. Further provided are methods for detecting excitatory glycine receptor ligands, agonists and antagonists. The invention also provides related diagnostic and therapeutic methods.
The present invention relates to novel 11-.beta. estradiol ester compounds and their use as locally active estrogens in the treatment of the symptomology of menopause and to treat estrogen sensitive cancers, including breast cancer.
The present invention provides methods for identifying patients at risk of developing preeclampsia. In further embodiments, the present invention relates to methods for the diagnosis of patients with preeclampsia.
The present invention relates to previously unknown biological roles of Nogo-B. We have discovered that Nogo-B is a component of endothelial cells. We have also discovered that Nogo-B is highly expressed in intact blood vessels. The amino terminus of Nogo-B promotes the adhesion, spreading and migration of endothelial cells and plays a role in vascular remodeling. Thus, Nogo-B is a novel regulator of vascular homeostasis and remodeling. The present invention provides compositions comprising Nogo-B and fragments and fusion proteins thereof. The present invention also relates to nucleic acids encoding Nogo-B and fragments and fusion proteins thereof, as well as vectors and cells comprising such nucleic acids. The present invention also relates to antibodies specific for Nogo-B and fragments and fusion proteins thereof. The present invention also provides methods for preventing, detecting and treating Nogo-B-related diseases, disorders and conditions.
Growth factor binding molecules having a plurality of peptide loops attached to a non-peptide organic scaffold, preferably having pseudo-six amino acid peptide loops with four amino acid sidechains. The growth factor binding molecules specifically bind various growth factors and are suitable for treating a subject having tumors or restinosis. In one embodiment a platelet-derived growth factor binding molecule is disclosed that is used to inhibit tumor growth and angiogenesis in solid tumors.
Exaggerated levels of VEGF are present in asthma. Transgenic mice that over-express VEGF exhibit an asthma-like phenotype with inflammation, parenchymal and vascular remodeling, edema, mucus metaplasia, myocyte hyperplasia, and airways hyper-responsiveness. VEGF also enhanced respiratory antigen sensitization and Th2 inflammation and increased the number of activated DC2 dendritic cells. Thus, VEGF is a mediator of inflammation that enhances antigen sensitization and plays a critical role in adaptive Th2 inflammation. A small molecule inhibitor of VEGF markedly decreased tissue inflammation and airway hyper-responsiveness. Similar results were seen with a soluble VEGF receptor trap. These inhibitors also markedly decreased antigen-stimulated IL-13 and IL-4 production. Therefore, VEGF inhibition may be therapeutic in asthma and other Th2 disorders.
Scientists at Yale have successfully demonstrated therapeutic efficacy of a monoclonal antibody targeting CCR5 in an animal model for Chronic Obstructive Pulmonary Disease (COPD).
A collaborative research effort, performed in part with Yale, has identified a unique method to induce the formation of new bone in targeted skeletal sites, as well as accelerate and secure the repair process of fractures.
Nogo-B is a newly-discovered protein that is highly expressed in endothelial and smooth muscle cells of the vessel wall. Nogo-B has been shown to be a regulator of cell migration in vitro and of vascular remodeling in vivo. Molecules that mimic the activity of Nogo-B have been shown to be pro-angiogenic. More recently, the receptor for Nogo-B has been identified. Antagonists of the receptor have been shown to be anti-angiogenic, and therefore useful for the treatment of solid tumors. Work at Yale is underway to identify additional anti-angiogenic molecules.
Few remedies exist to slow the ravages of old age such as Parkinsons, Alzheimer's, and osteoporosis. The lin-4 microRNA represses a molecule in the insulin signaling pathway, a pathway known to regulate lifespan in nematodes, flies and mice. Delivering this microRNA to humans will slow the effects of aging and assist in treating diseases of old age. MicroRNAs are natural human chemicals and hence microRNA treatments utilize a natural pathway which are likely to be more effective than other approaches.