Developed by Kazutaka Ikeda and Masami Mishina, Brain Research Institute, Niigata University in 1995. A pgk-neo was transfered into TT2 ES cells to replace the exon encoding the M4 putative transmembrane segment of Grin2d gene. The mutant mice were backcrossed to C57BL/6N over 10 times. B6.Cg-Grin2d<tm1Mim>/MimRbrc <a href="https://mus.brc.riken.jp/ja/wp-content/uploads/pdf/blc/01840_GB.pdf">Genetic Background</a> 条件を付加する。利用者は事前に寄託者の提供承諾書を得る。<br>研究成果の公表にあたって寄託者の指定する文献を引用する。Mol. Brain. Res., 33, 61-71 (1995).<br>研究成果の公表にあたって謝辞の表明を必要とする。<br>利用者が本リソースを用いて得た成果に基づき特許、知的所有権、または他の権利を申請する場合には、寄託者の同意を必要とする。本リソースの使用は共同研究のみに限定する。寄託後2 年以内の論文発表あるいは寄託後2 年以内に論文発表が無い場合はその後の論文発表の際には、利用者は寄託者を共著者とする必要がある。 GluR epsilon4 (Grin2d, glutamate receptor, ionotropic, NMDA2D (epsilon 4)) knockout mice. The Grin2d gene is one of the glutamate receptor channel subunit families forming NMDA receptor channel. The Grin2d homozygous mutant mice show a reduced spontaneous activity, but no significant difference in motor activity and anxiety tests when compared with normal mice. Reproductive performance and growth of them is normal. Masayoshi MISHINA 開発年：1995年開発者：池田和隆先生、三品昌美先生機関名：東京大学大学院医学系研究科薬理学分子神経生物学教室TT2 ES 細胞由来。C57BL/6N (日本クレア）と10世代戻し交配を行った。 NMDA 型グルタミン酸受容体 GluRε4 サブユニットを欠損したマウス。 GluRε4 KO mouse C (3-6 months) Heterozygote x Wild-type [C57BL/6NJcl]. Homozygous mutant mice are viable and fertile. Univ. Tokyo Necessary documents for ordering:<ol><li>Approval form (<A HREF="https://mus.brc.riken.jp/ja/wp-content/uploads/form/form_6.docx">Japanese</A> / <A HREF="https://mus.brc.riken.jp/en/wp-content/uploads/form/form_d.docx">English</A>)</li><li>Order form (<A HREF="https://mus.brc.riken.jp/ja/wp-content/uploads/form/form_4.docx">Japanese</A> / <A HREF="https://mus.brc.riken.jp/en/wp-content/uploads/form/form_b.docx">English</A>)</li><li>Category I MTA: MTA for distribution with RIKEN BRC (<A HREF="https://mus.brc.riken.jp/ja/wp-content/uploads/form/form_5.docx">Japanese</A> / <A HREF="https://mus.brc.riken.jp/en/wp-content/uploads/form/form_c.docx">English</A>)</li><li>Acceptance of responsibility for living modified organism (<A HREF="https://mus.brc.riken.jp/ja/wp-content/uploads/form/form_7.docx">Japanese</A> / <A HREF="https://mus.brc.riken.jp/en/wp-content/uploads/form/form_g.docx">English</A>)</li></ol> RBRC01840 The RECIPIENT of BIOLOGICAL RESOURCE shall obtain a prior written consent on use of it from the DEPOSITOR. In publishing the research results obtained by use of the BIOLOGICAL RESOURCE, a citation of the following literature(s) designated by the DEPOSITOR is requested. Mol. Brain. Res., 33, 61-71 (1995).In publishing the research results to be obtained by use of the BIOLOGICAL RESOURCE, an acknowledgment to the DEPOSITOR is requested. Prior to filing for a patent, or intellectual property or other rights based on results of research using the BIOLOGICAL RESOURCE, the RECIPIENT shall acquire the consent from the DEPOSITOR for such application. Use of the BIOLOGICAL RESOURCE shall be limited to a collaborative research. And Use of the BIOLOGICAL RESOURCE shall require co-authorship of the DEPOSITOR for TWO years after deposition of the BIOLOGICAL RESOURCE to the RIKEN BRC or for the first publication if no publication is made within the TWO years. 国立大学法人東京大学 E. coli neo, mouse phosphoglycerate kinase promoter (PGK promoter), mouse GluRε4 subunit genomic DNA Neurobiology Research C（3〜6か月） 三品　昌美 TT2 [(C57BL/6NCrlj x CBA/JNCrlj)F1] true 開発年：1995年 開発者：池田和隆先生、三品昌美先生 機関名：東京大学大学院医学系研究科薬理学分子神経生物学教室 TT2 ES 細胞由来。C57BL/6N (日本クレア）と10世代戻し交配を行った。 <a href='https://brc.riken.jp/mus/pcr01840'>Genotyping protocol -PCR-</a> GluRε4 KO mouse GluRε4 KO mouse ヘテロ同士の交配により系統維持。繁殖効率：A