開発年：1999年 開発者：清野裕先生（京都大学医学研究科病態代謝栄養学）
GIPR Knockout mice
GIPR Knockout mice
京都大学
C（3〜6か月）
mouse GIP receptor genomic DNA, E. coli neo, mouse phosphoglycerate kinase promoter (PGK promoter)
C (3-6 months)
特に問題なし。
<a href="https://mus.brc.riken.jp/ja/wp-content/uploads/pdf/blc/00782_GB.pdf">Genetic Background</a>
Yutaka SEINO
Developed by Dr. Yutaka Seino, Kyoto University in 1999. A neomycin cassette was inserted to replace exons 4 and 5 of GIPR gene. The mutant mice were backcrossed to C57BL/6.
GIPR Knockout mice
Kyoto Univ.
条件を付加する。<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。Miyawaki K, et al. Proc Natl Acad Sci USA, 96, 14843-14847 (1999).
当該マウスは、京大の清野先生の教室より入手後、C57BL/6 Cr Slc(日本エスエルシー) との掛け合わせを7世代行ったものです。それ以前に清野先生の教室においてもC57BL/6*との掛け合わせがあったと聞いておりますが、そちらの詳細は不明。
<a href='https://brc.riken.jp/mus/pcr00782'>Genotyping protocol -PCR-</a>
Backcross to C57BL/6 (Heterozygote x C57BL/6CrSlc)Homozygous mice are fertile and viable.
開発年：1999年開発者：清野裕先生（京都大学医学研究科病態代謝栄養学）
Necessary documents for ordering:<ol><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>
true
Backcross to C57BL/6 (Heterozygote x C57BL/6CrSlc) Homozygous mice are fertile and viable.
B6.129P2-Gipr<tm1Yse>/Rbrc
RBRC00782
清野 裕
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. Miyawaki K, et al. Proc Natl Acad Sci USA, 96, 14843-14847 (1999).
B6.129P2-Gipr<tm1Yse>. Gastric inhibitory polypeptide (GIP) is a gastrointestinal peptide hormone synthesized by K cells in the duodenum and small intestine, GIP plays a role in gastric secretory inhibition, gastric mobility, and insulin release by binding to its specific receptor, the GIP receptor (GIPR). Homozygous mutant mice for Gipr<tm1Yse> targeted mutation are fertile and viable, but exhibit hyperglycemia after high-fat diet ingestion. This strain is useful for elucidating of the signaling mechanism of GIP from pancreatic beta cell to intestine.