Abstract: It is an object to provide a gene-modified non-human animal having inactivated MGAT2 gene and a gene-modified non-human animal cell, which are useful for the search of the function of MGAT2 in vivo. It is another object to provide a method for screening of a compound capable of inhibiting the activity of MGAT2 and a compound capable of inhibiting the activity of MGAT2. It is further another object to provide a method for detecting a disease induced by abnormal lipid metabolism based on the expression level or activity of MGAT2. A method for screening of a compound by using a gene-modified non-human mammal having the artificially inhibited expression of MGAT2 gene and a cell thereof enable to prevent or treat a disease induced by abnormal lipid metabolism. Also a screening of a compound capable of inhibiting or enhancing the function of MGAT2 enables to prevent or treat a disease induced by abnormal lipid metabolism.

Abstract: The present inventors conducted a similarity search of the amino acid sequence of known G protein-coupled receptor proteins in GenBank, and obtained a novel human GPCR gene “BG37”, cDNA containing the ORF of the gene was cloned and its nucleotide sequence was determined. Moreover, novel GPCR “BG37” genes from mouse and rat were isolated. Use of the novel GPCR of the present invention enables screening of ligands, compounds inhibiting the binding to a ligand, and candidate compounds of pharmaceuticals which can regulate signal transduction from the “BG37” receptor.

Abstract: The present inventors conducted a similarity search of the amino acid sequence of known G protein-coupled receptor proteins in GenBank, and obtained a novel human GPCR gene “BG37”, cDNA containing the ORF of the gene was cloned and its nucleotide sequence was determined. Moreover, novel GPCR “BG37” genes from mouse and rat were isolated. Use of the novel GPCR of the present invention enables screening of ligands, compounds inhibiting the binding to a ligand, and candidate compounds of pharmaceuticals which can regulate signal transduction from the “BG37” receptor.

Abstract: The present inventors conducted a similarity search of the amino acid sequence of known G protein-coupled receptor proteins in GenBank, and obtained a novel human GPCR gene “BG37”. cDNA containing the ORF of the gene was cloned and its nucleotide sequence was determined. Moreover, novel GPCR “BG37” genes from mouse and rat were isolated. Use of the novel GPCR of the present invention enables screening of ligands, compounds inhibiting the binding to a ligand, and candidate compounds of pharmaceuticals which can regulate signal transduction from the “BG37” receptor.

Abstract: It is an object to provide a gene-modified non-human animal having inactivated MGAT2 gene and a gene-modified non-human animal cell, which are useful for the search of the function of MGAT2 in vivo. It is another object to provide a method for screening of a compound capable of inhibiting the activity of MGAT2 and a compound capable of inhibiting the activity of MGAT2. It is further another object to provide a method for detecting a disease induced by abnormal lipid metabolism based on the expression level or activity of MGAT2. A method for screening of a compound by using a gene-modified non-human mammal having the artificially inhibited expression of MGAT2 gene and a cell thereof enable to prevent or treat a disease induced by abnormal lipid metabolism. Also a screening of a compound capable of inhibiting or enhancing the function of MGAT2 enables to prevent or treat a disease induced by abnormal lipid metabolism.

Abstract: A Gpbar1-deficient mouse is constructed and it is examined whether or not Gpbar1 participates in the regulation of bile acid homeostasis and lipid metabolism. As a result, the total bile acid pool is decreased in the Gpbar1-deficient mouse without showing any change in the fecal bile acid level. A female Gpbar1-deficient mouse having been fed with a high fat feed shows a significant increase in body weight compared with a wild type mouse, which is caused by an increase in fat. These facts suggest that Gpbar1 contributes to the regulation of bile acid homeostasis and lipid metabolism.

Abstract: The present inventors conducted a similarity search of the amino acid sequence of known G protein-coupled receptor proteins in GenBank, and obtained a novel human GPCR gene “BG37”. cDNA containing the ORF of the gene was cloned and its nucleotide sequence was determined. Moreover, novel GPCR “BG37” genes from mouse and rat were isolated. Use of the novel GPCR of the present invention enables screening of ligands, compounds inhibiting the binding to a ligand, and candidate compounds of pharmaceuticals which can regulate signal transduction from the “BG37” receptor.

Abstract: The present inventors conducted a similarity search of the amino acid sequence of known G protein-coupled receptor proteins in GenBank, and obtained a novel human GPCR gene “BG37”. cDNA containing the ORF of the gene was cloned and its nucleotide sequence was determined. Moreover, novel GPCR “BG37” genes from mouse and rat were isolated. Use of the novel GPCR of the present invention enables screening of ligands, compounds inhibiting the binding to a ligand, and candidate compounds of pharmaceuticals which can regulate signal transduction from the “BG37” receptor.

Abstract: The present inventors conducted a similarity search of the amino acid sequence of known G protein-coupled receptor proteins in GenBank, and obtained a novel human GPCR gene “BG37”. cDNA containing the ORF of the gene was cloned and its nucleotide sequence was determined. Moreover, novel GPCR “BG37” genes from mouse and rat were isolated. Use of the novel GPCR of the present invention enables screening of ligands, compounds inhibiting the binding to a ligand, and candidate compounds of pharmaceuticals which can regulate signal transduction from the “BG37” receptor.