Abstract: A composition suitable for formulation of an enzymatic reaction mixture, the composition comprising a reaction component essential for an ex-vivo non-polymerase enzymatic reaction in which a substrate is catalyzed by an enzyme in a reaction mixture to form a product, and a tracer compatible with the enzyme, the composition being substantially free of the substrate.

Abstract: A composition suitable for formulation of an enzymatic reaction mixture, the composition comprising a reaction component essential for an ex-vivo non-polymerase enzymatic reaction in which a substrate is catalyzed by an enzyme in a reaction mixture to form a product, and a tracer compatible with the enzyme, the composition being substantially free of the substrate.

Abstract: A composition suitable for formulation of an enzymatic reaction mixture, the composition comprising a reaction component essential for an ex-vivo non-polymerase enzymatic reaction in which a substrate is catalyzed by an enzyme in a reaction mixture to form a product, and a tracer compatible with the enzyme, the composition being substantially free of the substrate.

Abstract: A composition suitable for formulation of an enzymatic reaction mixture, the composition comprising a reaction component essential for an ex-vivo non-polymerase enzymatic reaction in which a substrate is catalyzed by an enzyme in a reaction mixture to form a product, and a tracer compatible with the enzyme, the composition being substantially free of the substrate.

Abstract: The disclosure describes a unique animal model which is useful for studying the role of FGF14 in the central nervous system (CNS) and testing of potential drugs for treatment of CNS diseases. To provide this animal model, the Fgf14 gene is disrupted in mice by replacing the second and third exons with &bgr;-galactosidase. Neuropharmacological studies are disclosed which show that the Fgf14 deficient mice have disrupted striatal-nigra and striatal-pallidal pathways resulting in increased excitatory input to the cortex. The paroxysmal hyperkinetic disorder in Fgf14 deficient mice phenocopies a form of dystonia, a disease often associated with dysfunction of the putamen.

Abstract: A unique animal model is disclosed which is useful for studying the role of FGF-9 activity in cardiovascular diseases. To provide this animal model, the FGF-9 gene is disrupted in mice, that is, null mutation in the mouse FGF-9 gene is engineered. This knockout mouse was produced by deleting the sequences immediately downstream of the initiation methionine in exon 1. Analysis of the FGF-9 null embryos demonstrates perinatal lethality with apparent pathology in lung and cardiac tissue.

Abstract: Disclosed are fibroblast growth factor (FGF) binding and FGF receptor activation, and a method of identifying small molecular weight compounds that interact with FGF to modulate its activity such as, e.g., activators and inhibitors. Illustrative small oligosaccharides, namely di- and tri-saccharides, are shown to be effective modulators of FGF binding and FGF receptor activation.

Abstract: A homogeneous population of cells having on average (1) a number of cell surface low-affinity heparin-binding growth factor (HBGF) sites per cell less than 20% of the number of such binding sites found on wild-type CHO-K1 cells (ATCC Accession No. CCL61), and at least three times the number of cell surface high-affinity HBGF receptors per cell found on such CHO-K1 cells; and an assay system utilizing such cells.

Abstract: Disclosed are fibroblast growth factor (FGF) binding and FGF receptor activation, and a method of identifying small molecular weight compounds that interact with FGF to modulate its activity such as, e.g., activators and inhibitors. Illustrative small oligosaccharides, namely di- and tri-saccharides, are shown to be effective modulators of FGF binding and FGF receptor activation.

Abstract: A homogeneous population of cells having on average (1) a number of cell surface low-affinity heparin-binding growth factor (HBGF) sites per cell less than 20% of the number of such binding sites found on wild-type CHO-K1 cells (ATCC Accession No. CCL61), and at least three times the number of cell surface high-affinity HBGF receptors per cell found on such CHO-K1 cells; and an assay system utilizing such cells.