Title:
痛風発症素因の評価方法
Document Type and Number:
Japanese Patent JP6628226
Kind Code:
B2
Abstract:
To specify a molecule associated with the onset of gout so as to provide a method for evaluating a diathesis of uric acid-related diseases and a diathesis of inflammation-related diseases, an evaluation kit for carrying out the method, an inspection object, and a drug, on the basis of the molecule specified above, for contributing to the early treatment and prevention of the uric acid-related diseases and inflammation-related diseases. The molecule includes any one protein and cDNA of CNIH2-PACS1, ALDH2, MYL2-CUX2, GCKR, MAP3K11, NPT4, ABCG2, HIST1H2BF/HIST1H4E, HIST1H2BE/HIST1H4D and FAM35A, or proteins of combination thereof with GLUT9, NPT1, URAT1, or NXRN2, and is capable of selectively inducing gout. A molecule includes protein and cDNA of an ABCG2 variant and is capable of selectively and ATP-dependently decreasing urate excretion.
Inventors:
Hirotaka Matsuo
Ryuhei Takada
Shinnomiya
Ryuhei Takada
Shinnomiya
Application Number:
JP2015557911A
Publication Date:
January 08, 2020
Filing Date:
January 19, 2015
Export Citation:
Assignee:
Hirotaka Matsuo
National University Corporation Tokyo University
Shinnomiya
National University Corporation Tokyo University
Shinnomiya
International Classes:
C12Q1/6827; C07K14/47; C12N15/12; G01N33/68
Domestic Patent References:
| JP2011097926A | ||||
| JP2013500018A | ||||
| JP2012244990A | ||||
| JP2007060967A |
Foreign References:
| WO2004078130A1 | ||||
| WO2010150525A1 | ||||
| WO2013056132A1 | ||||
| US20100248253 | ||||
| US20100035255 |
Other References:
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ANALYSIS OF THE GENOTYPES FOR ALDEHYDE DEHYDROGENASE 2 IN JAPANESE PATIENTS WITH PRIMARY GOUT,Advances in Experimental Medicine and Biology, 1994, Vol.370, P.53-56
Genetic Impact on Uric Acid Concentration and Hyperuricemia in the Japanese Population,J. Atheroscler Thromb., 2013, Vol.20, No.4, P.351-367
腎における尿酸輸送の関係について教えてください,腎と透析, 2012, Vol.73, No.3, P.397-400
A Na+-phosphate cotransporter homologue (SLC17A4 protein) is an intestinal organic anion exporter,Am. J. Physiol. Cell Physiol., 2012, Vol.302, P.C1652-C1660
Common Defects of ABCG2, a High-Capacity Urate Exporter, Cause Gout: A Function-Based Genetic Analysis in a Japanese Population, Science Translational Medicine, 2009, Vol.1, Issue 5, P.1-8
Common dysfunctional variants in ABCG2 are a major cause of early-onset gout, Scientific Reports, 2013, 3:2014, P.1-4
Decreased extra-renal urate excretion is a common cause of hyperuricemia,Nature Communications, 2012, Vol.3:764, P.1-7
Genome Analysis Identifies the p15ink4b Tumor Suppressor as a Direct Target of the ZNF217/CoREST Complex,Mol. Cell Biol., 2008, Vol.28, No.19, P.6066-6077
Molecular identification of a renal urate-anion exchanger that regulates blood urate levels,Nature, 2002, Vol.417, P.447-452
Mutations in Glucose Transporter 9 Gene SLC2A9 Cause Renal Hypouricemia,American Journal of Human Genetics, 2008, Vol.83, P.744-751
Genome-wide association study for serum urate concentrations and gout among African Americans identifies genomic risk loci and a novel URAT1 loss-of-function allele, Human Molecular Genetics, 2011, Vol.20, No.20, P.4056-4068
Genome-wide association analyses identify 18 new loci associated with serum urate concentrations,Nature Genetics, 2013, Vol.45, No.2, P.145-154
Drug Metab Parmacokinet, 2007, vol.22, no.6, p.428-440
ANALYSIS OF THE GENOTYPES FOR ALDEHYDE DEHYDROGENASE 2 IN JAPANESE PATIENTS WITH PRIMARY GOUT,Advances in Experimental Medicine and Biology, 1994, Vol.370, P.53-56
Genetic Impact on Uric Acid Concentration and Hyperuricemia in the Japanese Population,J. Atheroscler Thromb., 2013, Vol.20, No.4, P.351-367
腎における尿酸輸送の関係について教えてください,腎と透析, 2012, Vol.73, No.3, P.397-400
A Na+-phosphate cotransporter homologue (SLC17A4 protein) is an intestinal organic anion exporter,Am. J. Physiol. Cell Physiol., 2012, Vol.302, P.C1652-C1660
Common Defects of ABCG2, a High-Capacity Urate Exporter, Cause Gout: A Function-Based Genetic Analysis in a Japanese Population, Science Translational Medicine, 2009, Vol.1, Issue 5, P.1-8
Common dysfunctional variants in ABCG2 are a major cause of early-onset gout, Scientific Reports, 2013, 3:2014, P.1-4
Decreased extra-renal urate excretion is a common cause of hyperuricemia,Nature Communications, 2012, Vol.3:764, P.1-7
Genome Analysis Identifies the p15ink4b Tumor Suppressor as a Direct Target of the ZNF217/CoREST Complex,Mol. Cell Biol., 2008, Vol.28, No.19, P.6066-6077
Molecular identification of a renal urate-anion exchanger that regulates blood urate levels,Nature, 2002, Vol.417, P.447-452
Mutations in Glucose Transporter 9 Gene SLC2A9 Cause Renal Hypouricemia,American Journal of Human Genetics, 2008, Vol.83, P.744-751
Genome-wide association study for serum urate concentrations and gout among African Americans identifies genomic risk loci and a novel URAT1 loss-of-function allele, Human Molecular Genetics, 2011, Vol.20, No.20, P.4056-4068
Genome-wide association analyses identify 18 new loci associated with serum urate concentrations,Nature Genetics, 2013, Vol.45, No.2, P.145-154
Drug Metab Parmacokinet, 2007, vol.22, no.6, p.428-440
Attorney, Agent or Firm:
Hitoshi Shinbo