Abstract: The invention relates among others to a protein comprising a fragment of 30-240 amino acids of Collagen and calcium-binding EGF domain-containing protein 1 (CCBE1) having 0-10 amino acid substitutions with respect to the amino acid sequence of SEQ ID NO: 1, wherein said fragment comprises at least a collagen domain of CCBE1, or a variant thereof comprising 1, 2 or 3 amino acid substitutions. The invention further describes means and methods for the treatment of individuals with the protein or protein binding thereto.

Abstract: Human MYLK genes are identified as modulators of branching morphogenesis, and thus are therapeutic targets for disorders associated with defective branching morphogenesis function. Methods for identifying modulators of branching morphogenesis, comprising screening for agents that modulate the activity of MYLK are provided.

Abstract: The invention relates to a method for testing whether a compound is capable of inhibiting the development of lymphatic channels or lymphangiogenesis and/or the migration of lymphangioblasts in an non-human animal, a non-human embryo or a cell culture, comprising steps of contacting a compound capable of interacting with a Ccbe1 gene, a transcript thereof or a ccbe1 protein with a non-human animal, a non-human embryo or a cell culture; determining whether said compound inhibits the development of lymphatic channels, lymphangiogenesis and/or migration of lymphangioblasts in said non-human animal, a non-human embryo or a cell culture. The invention further related to a method of determining whether an individual is a carrier of, or is suffering from, or at risk of suffering from, a lymph vessel disorder, and to a medicament comprising Ccbe1, or comprising a nucleic acid encoding Ccbe1, for the treatment of a lymph vessel disorder.

Abstract: Human MYLK genes are identified as modulators of branching morphogenesis, and thus are therapeutic targets for disorders associated with defective branching morphogenesis function. Methods for identifying modulators of branching morphogenesis, comprising screening for agents that modulate the activity of MYLK are provided.

Abstract: Human MBM genes are identified as modulators of branching morphogenesis, and thus are therapeutic targets for disorders associated with defective branching morphogenesis function. Methods for identifying modulators of branching morphogenesis, comprising screening for agents that modulate the activity of MBM are provided.

Abstract: Human NADK genes are identified as modulators of branching morphogenesis, and thus are therapeutic targets for disorders associated with defective branching morphogenesis function. Methods for identifying modulators of branching morpho-genesis, comprising screening for agents that modulate the activity of NADK are provided.

Abstract: Human MAPK7 genes are identified as modulators of branching morphogenesis, and thus are therapeutic targets for disorders associated with defective branching morphogenesis function. Methods for identifying modulators of branching morphogenesis, comprising screening for agents that modulate the activity of MAPK7 are provided.

Abstract: Human CDKL1 genes are identified as modulators of branching morphogenesis, and thus are therapeutic targets for disorders associated with defective branching morphogenesis function. Methods for identifying modulators of branching morphogenesis, comprising screening for agents that modulate the activity of CDKL1 are provided.

Abstract: An engineered mutant teleost embryo having reduced flt1 activity that causes a phenotype of normal assembly of main circulatory routes and a reduction in sprouted blood vessels is described. Methods of using the mutant teleost embryo for identifying genes that interact with flt1 are also described.