Abstract: Methods of treating and/or inhibiting a bone morphogenetic protein (BMP)-related disorder or condition by administering a BMP antagonist to a subject suffering from a BMP-related disorder or condition such that the BMP-related disorder or condition is treated. The method is carried out with a human noggin or a human noggin deletion mutant.

Abstract: Nucleic acid molecules and multimeric proteins capable of binding vascular endothelial growth factor (VEGF). VEGF traps are disclosed which are therapeutically useful for treating VEGF-associated conditions and diseases, and are specifically designed for local administration to specific organs, tissues, and/or cells.

Abstract: Human Cerberus proteins and related nucleic acids are provided. Included are proteins comprising a human cerberus domain having specific activity, particularly the ability to antagonize a bone morphogenic protein. The proteins may be produced recombinantly from transformed host cells with the subject nucleic acids. Also provided are isolated hybridization probes and primers capable of specifically hybridizing with the disclosed genes, specific binding agents and methods of making and using the subject compositions.

Abstract: Methods of creating mutations in genomic exons by inserting introns into the genomic exons via homologous recombination. Also, methods are provided for introducing modifications into genomic exons by inserting introns into the genomic exons via homologous recombination such that a mature mRNA transcript produced from a genomic region of the genome comprising the genomic exon does not contain the modification are provided. The methods provide for a rapid method for introducing mutations and/or modifications of any type into a mammalian cell genome.

Abstract: The present invention provides for nucleic acid sequences that encode novel mammalian intracellular signaling polypeptides, designated MINC102. The invention also provides assay systems that may be used to detect and/or measure agents that bind the MINC102 gene product. The present invention also provides for diagnostic and therapeutic methods for treating muscle atrophy by inhibiting expression or activity of MINC102.

Abstract: Modified ciliary neurotrophic factor, methods for production and methods of use, especially in the treatment of Huntington's disease, obesity, and gestational or adult onset diabetes.

Abstract: A method for engineering and utilizing large DNA vectors to target, via homologous recombination, and modify, in any desirable fashion, endogenous genes and chromosomal loci in eukaryotic cells. These large DNA targeting vectors for eukaryotic cells, termed LTVECs, are derived from fragments of cloned genomic DNA larger than those typically used by other approaches intended to perform homologous targeting in eukaryotic cells. Also provided is a rapid and convenient method of detecting eukaryotic cells in which the LTVEC has correctly targeted and modified the desired endogenous gene(s) or chromosomal locus (loci) as well as the use of these cells to generate organisms bearing the genetic modification.

Abstract: Nucleic acid molecules and multimeric proteins capable of binding vascular endothelial growth factor (VEGF). VEGF mini-traps are disclosed which are therapeutically useful for treating VEGF-associated conditions and diseases, and are specifically designed for local administration to specific organs, tissues, and/or cells.

Abstract: The present invention provides a fusion polypeptide that forms a multimer that is capable of binding a cytokine to form a nonfunctional complex. It also provides a nucleic acid sequence encoding the fusion polypeptide and methods of making and uses for the fusion polypeptide.

Abstract: High affinity fusion proteins (“trapbodies”), capable of binding and inhibiting the activity of soluble, interacting proteins (“SIPs”) are described. The trapbodies are multimers, preferably dimers, of SIP-specific fusion polypeptides which comprise SIP binding domains derived from SIP targets and/or anti-SIP immunoglobulins, as well as multimerizing components.

Abstract: Modified chimeric polypeptides with improved pharmacokinetics are disclosed. Specifically, modified chimeric Flt1 receptor polypeptides that have been modified in such a way as to improve their pharmacokinetic profile are disclosed. Also disclosed are methods of making and using the modified polypeptides including but not limited to using the modified polypeptides to decrease or inhibit plasma leakage and/or vascular permeability in a mammal.

Abstract: The present invention provides for an isolated nucleic acid molecule encoding a human TIE-2 ligand. In addition, the invention provides for a receptorbody which specifically binds a human TIE-2 ligand. The invention also provides an antibody which specifically binds a human TIE-2 ligand. The invention further provides for an antagonist of human TIE-2. The invention further provides for a ligandbody which specifically binds TIE-2 receptor. The invention also provides for therapeutic compositions as well as a method of blocking blood vessel growth, a method of promoting neovascularization, a method of promoting the growth, differentiation or migration of cells expressing the TIE-2 receptor, including, but not limited to, hematopoietic precursor cells, a method of blocking the growth, differentiation or migration of cells expressing the TIE-2 receptor including, but not limited to, hematopoietic precursor cells, and a method of attenuating or preventing tumor growth in a human.

Abstract: The present invention provides for an isolated nucleic acid molecule encoding a human TIE-2 ligand. In addition, the invention provides for a receptor body which specifically binds a human TIE-2 ligand. The invention also provides an antibody which specifically binds a human TIE-2 ligand. The invention further provides for an antagonist of human TIE-2. The invention also provides for therapeutic compositions as well as a method of blocking blood vessel growth, a method of promoting neovascularization, a method of promoting the growth or differentiation of a cell expressing the TIE-2 receptor, a method of blocking the growth or differentiation of a cell expressing the TIE-2 receptor and a method of attenuating or preventing tumor growth in a human.

Abstract: Peptides that specifically interfere with the ability of VEGF165 to interact with the NP-1 receptor or with a VEGFR-2/NP-1 co-receptor complex are disclosed. The inventive peptides are useful to control pathological angiogenesis, such as occurs in cancer and other diseases. The peptides are based on a combination of basic residues contained within Exon 6 of human placental growth factor (PIGF), coupled at the carboxyl terminus to either Exon 8 of VEGF165 or Exon 7 of PIGF. The peptides behave as antagonists of VEGF165 signaling through a mechanism that involves competition for VEGF165 binding at either the VEGFR-2/NP-1 complex or NP-1, without affecting VEGF signaling through other pathways. This binding is sufficient to attenuate pathological angiogenesis such as occurs in tumor growth.

Abstract: Methods of treating diabetes in mammals, particularly humans, by blocking or inhibiting VEGF-mediated activity. A preferred inhibitor of VEGF-mediated activity is a VEGF antagonist such as a VEGF trap capable of binding and blocking VEGF.

Abstract: The invention generally relates to angiogenic factors and more particularly to the angiopoietin family of growth factors and to methods of using these growth factors to induce vasodilation and hypotension and reducing hypertension.

Abstract: The present invention provides for a modified TIE-2 ligand 2 which has been altered by addition, deletion or substitution of one or more amino acids, or by way of tagging, with for example, the Fc portion of human IgG-1, but which retains its ability to bind the TIE-2 receptor.

Abstract: Novel fusion polypeptide ligands that bind Eph family receptors or the Tie-2 receptor are identified, and methods for making the fusion polypeptide ligands in biologically active form are described. Nucleic acids encoding these novel fusion polypeptide ligands enable production of the fusion polypeptide ligands. The method of making the nucleic acids and the fusion polypeptide ligands is broadly applicable to the production of polypeptide ligands in general, resulting in improved affinity and/or increased activity of the ligand when compared to its native form.

Abstract: Methods for imaging and targeting tumor vasculature are provided. Specifically, the methods for imaging and targeting tumor vasculature relate to using ephrin-B2 to image developing tumor vasculature and to target therapeutic agents to developing tumor vasculature. Kits for imaging and targeting tumor vasculature are also provided. Also provided for are methods of delivering agents to vasculature.

Abstract: The present invention relates to neurotrophin-3 (NT-3), a newly discovered member of the BDNF gene family. It is based, in part, on the identification of regions of nucleic acid sequence homology shared by BDNF and NGF (U.S. patent application Ser. No. 07/400,591, filed Aug. 30, 1989, incorporated by reference herein). According to the present invention, these regions of homology may be used to identify new members of the BDNF/NGF gene family; such methodology was used to identify NT-3. The present invention provides for the genes and gene products of new BDNF/NGF related neurotrophic factors identified by these methods. According to the invention, NT-3 may be used in the diagnosis and/or treatment of neurologic disorders, including, but not limited to, Alzheimer's disease and Parkinson's disease. Because NT-3 has been observed to exhibit a spectrum of activity different from the spcificities of BDNF or NGF, NT-3 provides new and valuable options for enducing regrowth and repair in the central nervous system.