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KNOCK-IN MOUSE UPDATE コモンズ

外国特許コード F150008196
掲載日 2015年3月24日
出願国 世界知的所有権機関(WIPO)
国際出願番号 2014JP053555
国際公開番号 WO 2014126225
国際出願日 平成26年2月14日(2014.2.14)
国際公開日 平成26年8月21日(2014.8.21)
優先権データ
  • 特願2013-026838 (2013.2.14) JP
発明の名称 (英語) KNOCK-IN MOUSE UPDATE コモンズ
発明の概要(英語) The present invention addresses the problem of providing a knock-in mouse that develops Osaka-mutation-mediated Alzheimer's disease through gene expression in normal physiological ranges. The problem is solved by a knock-in mouse as described below. A knock-in mouse into which a mutant amyloid precursor protein (mutant APP) gene described in (a) or (b), below, has been introduced, said mouse being homozygous for the mutant APP gene. (a) A mutant APP gene that codes a mutant murine amyloid-β protein and comprises the amino acid sequence represented by SEQ ID NO: 1. (b) A mutant APP gene that codes a polypeptide which induces the onset of Alzheimer's disease when expressed in mice, said gene comprising the amino acid sequence represented by SEQ ID NO: 1, in which one or more amino acids other than the 5th glutamine residue from the N terminal, the 10th phenylalanine residue from the N terminal and the 13th arginine residue from the N terminal has/have been substituted, deleted, inserted or added.
従来技術、競合技術の概要(英語) BACKGROUND ART
Conventional, Alzheimer's disease, amyloid β protein and accumulated fibrosis, by forming the senile plaques has been considered to develop. Amyloid β is, one or 770 695 amino acid residues of the amyloid precursor protein (APP) by beta-secretase is cut out a part of the amino acid residues about 40 generated by the high aggregation properties of the peptide. However, in recent years, senile plaque formation is not the cause of Alzheimer's disease, amyloid β protein oligomer Alzheimer's true etiological hypothesis and has attracted attention (for example see non-patent document 1 and the like).
The inventors of the present invention, oligomers of amyloid β protein facilitating the formation of a type found Alzheimer's disease patient having a mutation, this mutation was named Osaka (for example see non-patent document 2). 42 Or 40 amino acid residues Osaka mutations amyloid β protein can be residues of glutamic acid residues are deleted on the basis of the 22 mutations, amyloid β protein of this mutation is also less likely to fibrosis, oligomer formation is believed to be promoted.
The main cause of dementia is Alzheimer's disease patients increase, in recent years, a great social concern and, at an early stage of the treatment methods of the therapeutic drugs are desired to establish. Treat a specific disease drugs or therapeutic method for this examination, analysis using animal models of the disease is carried out in general. The present inventor et al., Osaka APP gene having a mutation introduced into the human mutant form, has a mutation in the amyloid β protein Osaka human transgenic mice that overexpress the was produced. However, the results obtained are transgenic mice, expression of the introduced gene has been introduced or extraneous artifact caused by the possibility cannot be denied. Further, human-type APP gene has been introduced for murine, human type of amyloid β protein is expressed in mice and, cannot be accurately heterologous interaction between negative pathology may not be reflected in the.
The problem of such heterologous interaction, a mutant amyloid β in mice the type which produces a protein to create a model Alzheimer's disease can be avoided by. However, conventional, mouse-type amyloid β protein is a human type is generally behaves differently and has been considered. Amyloid β protein is, in the humanized mouse-type variations in amino acid residues 3, due to differences in the amino acid residues of the amyloid β protein and hardly causes the accumulation of the results of the experiment is reported (for example see non-patent document 3). In addition, a method of treatment or a therapeutic agent against a normally a human body in order to study the transgenic animal is utilized, the introduction of human genes and understood and should have, a mutant amyloid β mouse-type mice deliberately introduced a gene encoding a protein to create a model can be Alzheimer's disease has not been investigated. Therefore, a protein derived from human gene does not have a mouse-type genetic information, or mouse-type Alzheimer's disease model mouse abnormal protein alone has not been reported in the present circumstances.
  • 出願人(英語)
  • ※2012年7月以前掲載分については米国以外のすべての指定国
  • OSAKA CITY UNIVERSITY
  • 発明者(英語)
  • MORI, Hiroshi
  • TOYAMA, Takami
  • UMEDA, Tomohiro
  • MORITA, Takashi
  • YOSHIDA, Kayo
国際特許分類(IPC)
指定国 National States: AE AG AL AM AO AT AU AZ BA BB BG BH BN BR BW BY BZ CA CH CL CN CO CR CU CZ DE DK DM DO DZ EC EE EG ES FI GB GD GE GH GM GT HN HR HU ID IL IN IR IS JP KE KG KN KP KR KZ LA LC LK LR LS LT LU LY MA MD ME MG MK MN MW MX MY MZ NA NG NI NO NZ OM PA PE PG PH PL PT QA RO RS RU RW SA SC SD SE SG SK SL SM ST SV SY TH TJ TM TN TR TT TZ UA UG US UZ VC VN ZA ZM ZW
ARIPO: BW GH GM KE LR LS MW MZ NA RW SD SL SZ TZ UG ZM ZW
EAPO: AM AZ BY KG KZ RU TJ TM
EPO: AL AT BE BG CH CY CZ DE DK EE ES FI FR GB GR HR HU IE IS IT LT LU LV MC MK MT NL NO PL PT RO RS SE SI SK SM TR
OAPI: BF BJ CF CG CI CM GA GN GQ GW KM ML MR NE SN TD TG

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