Abstract: A novel class or family of TGF-? binding proteins is disclosed. Also disclosed are assays for selecting molecules for increasing bone mineralization and methods for utilizing such molecules.

Abstract: A novel class or family of TGF-? binding proteins is disclosed. Also disclosed are assays for selecting molecules for increasing bone mineralization and methods for utilizing such molecules.

Abstract: Described herein are pharmaceutical compositions comprising an anti-sclerostin antibody and an inhibitor of bone resorption.

Abstract: The genomic locus responsible for Van Buchem's disease is narrowed to an approximately 92 kb region of human chromosome 17 at 17q21. Individuals afflicted with or carriers of Van Buchem's disease exhibit a 52 kb deletion within this 92 kb region. Methods are provided that permit the differentiation between individuals homozygous for and therefore afflicted with Van Buchem's disease, individuals heterozygous for and therefore carriers of Van Buchem's disease, and individuals who are normal with respect to Van Buchem's disease. Also provided are general methodologies for the detection of a wide variety of large genomic deletions.

Abstract: A novel class or family of TGF-? binding proteins is disclosed. Also disclosed are assays for selecting molecules for increasing bone mineralization and methods for utilizing such molecules.

Abstract: A novel class or family of TGF-? binding proteins is disclosed. Also disclosed are assays for selecting molecules for increasing bone mineralization and methods for utilizing such molecules.

Abstract: A novel class or family of TGF-? binding proteins is disclosed. Also disclosed are assays for selecting molecules for increasing bone mineralization and methods for utilizing such molecules.

Abstract: The genomic locus responsible for Van Buchem's disease is narrowed to an approximately 92 kb region of human chromosome 17 at 17q21. Individuals afflicted with or carriers of Van Buchem's disease exhibit a 52 kb deletion within this 92 kb region. Methods are provided that permit the differentiation between individuals homozygous for and therefore afflicted with Van Buchem's disease, individuals heterozygous for and therefore carriers of Van Buchem's disease, and individuals who are normal with respect to Van Buchem's disease. Also provided are general methodologies for the detection of a wide variety of large genomic deletions.

Abstract: Compositions and methods are provided for determining in a subject a risk for having, or presence of, altered bone mineral density such as osteoporosis or osteopenia or other conditions characterized by decreased or increased bone density. Specifically, the invention relates to determination of a sclerostin gene region nucleotide polymorphism (SRP) in DNA of the sclerostin gene region of human chromosome 17. In certain embodiments, SRPs that indicate an increased risk for altered bone mineral density occur as gender-associated polymorphisms. Isolated polynucleotides comprising representative SRPs are also provided.

Abstract: Compositions and methods for increasing bone density using antibodies directed to a novel class or family of TGF-? binding proteins are provided. The disclosed compositions are useful, for example, in the diagnosis, prevention and/or treatment of diseases associated with a loss of bone density, for example osteoporosis.

Abstract: The genomic locus responsible for Van Buchem's disease is narrowed to an approximately 92 kb region of human chromosome 17 at 17q21. Individuals afflicted with or carriers of Van Buchem's disease exhibit a 52 kb deletion within this 92 kb region. Methods are provided that permit the differentiation between individuals homozygous for and therefore afflicted with Van Buchem's disease, individuals heterozygous for and therefore carriers of Van Buchem's disease, and individuals who are normal with respect to Van Buchem's disease. Also provided are general methodologies for the detection of a wide variety of large genomic deletions.

Abstract: A novel class or family of TGF-? binding proteins is disclosed. Also disclosed are assays for selecting molecules for increasing bone mineralization and methods for utilizing such molecules.

Abstract: A novel class or family of TGF-? binding proteins is disclosed. Also disclosed are assays for selecting molecules for increasing bone mineralization and methods for utilizing such molecules.

Abstract: Antibodies to a novel family of TGF-? binding proteins are disclosed, for use in methods of altering bone density and bone mineralization, which methods are applicable to the treatment of diseases including osteopenia and osteoporosis.

Abstract: Compositions and methods for increasing bone density using antibodies directed to a novel class or family of TGF-&bgr; binding proteins are provided. The disclosed compositions are useful, for example, in the diagnosis, prevention and/or treatment of diseases associated with a loss of bone density, for example osteoporosis.

Abstract: A novel class or family of TGF-&bgr; binding proteins is disclosed. Also disclosed are assays for selecting molecules for increasing bone mineralization and methods for utilizing such molecules.

Abstract: A novel class or family of TGF-&bgr; binding proteins is disclosed. Also disclosed are assays for selecting molecules for increasing bone mineralization and methods for utilizing such molecules. In particular, compositions and methods relating to antibodies that specifically bind to TGF-beta binding proteins are provided. These methods and compositions relate to altering bone mineral density by interfering with the interaction between a TGF-beta binding protein sclerostin and a TGF-beta superfamily member, particularly a bone morphogenic protein. Increasing bone mineral density has uses in diseases and conditions in which low bone mineral density typifies the condition, such as osteopenia, osteoporosis, and bone fractures.

Abstract: Compositions and methods are provided for determining in a subject a risk for having, or presence of, altered bone mineral density such as osteoporosis or osteopenia or other conditions characterized by decreased or increased bone density. Specifically, the invention relates to determination of a sclerostin gene region nucleotide polymorphism (SRP) in DNA of the sclerostin gene region of human chromosome 17. In certain embodiments, SRPs that indicate an increased risk for altered bone mineral density occur as gender-associated polymorphisms. Isolated polynucleotides comprising representative SRPs are also provided.

Abstract: A novel class or family of TGF-&bgr; binding proteins is disclosed. Also disclosed are assays for selecting molecules for increasing bone mineralization and methods for utilizing such molecules.

Abstract: The genomic locus responsible for Van Buchem's disease is narrowed to an approximately 92 kb region of human chromosome 17 at 17q21. Individuals afflicted with or carriers of Van Buchem's disease exhibit a 52 kb deletion within this 92 kb region. Methods are provided that permit the differentiation between individuals homozygous for and therefore afflicted with Van Buchem's disease, individuals heterozygous for and therefore carriers of Van Buchem's disease, and individuals who are normal with respect to Van Buchem's disease. Also provided are general methodologies for the detection of a wide variety of large genomic deletions.