Item type |
デフォルトアイテムタイプ(フル)(1) |
公開日 |
2020-11-20 |
タイトル |
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タイトル |
Mutations in the C1 element of the insulin promoter lead to diabetic phenotypes in homozygous mice |
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言語 |
en |
作成者 |
Noguchi, Hirofumi
Miyagi-Shiohira, Chika
Nakashima, Yoshiki
Kinjo, Takao
Saitoh, Issei
Watanabe, Masami
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アクセス権 |
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アクセス権 |
open access |
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アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
権利情報 |
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言語 |
en |
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権利情報 |
Creative Commons Attribution 4.0 |
権利情報 |
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言語 |
en |
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権利情報Resource |
https://creativecommons.org/licenses/by/4.0/ |
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権利情報 |
https://creativecommons.org/licenses/by/4.0/ |
内容記述 |
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内容記述タイプ |
Other |
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内容記述 |
Genome editing technologies such as CRISPR–Cas9 are widely used to establish causal associations between mutations and phenotypes. However, CRISPR–Cas9 is rarely used to analyze promoter regions. The insulin promoter region (approximately 1,000 bp) directs β cell-specific expression of insulin, which in vitro studies show is regulated by ubiquitous, as well as pancreatic, β cell-specific transcription factors. However, we are unaware of any confirmatory in vivo studies. Here, we used CRISPR–Cas9 technology to generate mice with mutations in the promoter regions of the insulin I (Ins1) and II (Ins2) genes. We generated 4 homozygous diabetic mice with 2 distinct mutations in the highly conserved C1 elements in each of the Ins1 and Ins2 promoters (3 deletions and 1 replacement in total). Remarkably, all mice with homozygous or heterozygous mutations in other loci were not diabetic. Thus, the C1 element in mice is required for Ins transcription in vivo. |
内容記述 |
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内容記述タイプ |
Other |
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内容記述 |
論文 |
出版者 |
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言語 |
en |
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出版者 |
Springer Nature |
言語 |
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言語 |
eng |
資源タイプ |
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資源タイプ |
journal article |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
出版タイプ |
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出版タイプ |
VoR |
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出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
識別子 |
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識別子 |
http://hdl.handle.net/20.500.12000/47285 |
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識別子タイプ |
HDL |
関連情報 |
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識別子タイプ |
DOI |
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関連識別子 |
https://doi.org/10.1038/s42003-020-1040-z |
関連情報 |
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識別子タイプ |
DOI |
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関連識別子 |
https://doi.org/10.1038/s42003-020-1040-z |
収録物識別子 |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
2399-3642 |
収録物名 |
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言語 |
en |
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収録物名 |
Communications Biology |
書誌情報 |
巻 3,
発行日 2020-06-16
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