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Title: Direct reprogramming of somatic cells is promoted by maternal transcription factor Glis1.
Authors: Maekawa, Momoko
Yamaguchi, Kei
Nakamura, Tomonori  kyouindb  KAKEN_id  orcid (unconfirmed)
Shibukawa, Ran
Kodanaka, Ikumi
Ichisaka, Tomoko
Kawamura, Yoshifumi
Mochizuki, Hiromi
Goshima, Naoki
Yamanaka, Shinya  kyouindb  KAKEN_id
Author's alias: 前川, 桃子
山中, 伸弥
Issue Date: 9-Jun-2011
Publisher: Nature Publishing Group
Citation: Maekawa M, Yamaguchi K, Nakamura T, Shibukawa R, Kodanaka I, Ichisaka T, Kawamura Y, Mochizuki H, Goshima N, Yamanaka S. Direct reprogramming of somatic cells is promoted by maternal transcription factor Glis1. Nature. 2011 Jun 8;474(7350):225-9. doi: 10.1038/nature10106.
Journal title: Nature
Volume: 474
Issue: 7350
Start page: 225
End page: 229
Abstract: Induced pluripotent stem cells (iPSCs) are generated from somatic cells by the transgenic expression of three transcription factors collectively called OSK: Oct3/4 (also called Pou5f1), Sox2 and Klf4. However, the conversion to iPSCs is inefficient. The proto-oncogene Myc enhances the efficiency of iPSC generation by OSK but it also increases the tumorigenicity of the resulting iPSCs. Here we show that the Gli-like transcription factor Glis1 (Glis family zinc finger 1) markedly enhances the generation of iPSCs from both mouse and human fibroblasts when it is expressed together with OSK. Mouse iPSCs generated using this combination of transcription factors can form germline-competent chimaeras. Glis1 is enriched in unfertilized oocytes and in embryos at the one-cell stage. DNA microarray analyses show that Glis1 promotes multiple pro-reprogramming pathways, including Myc, Nanog, Lin28, Wnt, Essrb and the mesenchymal-epithelial transition. These results therefore show that Glis1 effectively promotes the direct reprogramming of somatic cells during iPSC generation.
Description: 転写因子Glis1により安全なiPS細胞の高効率作製に成功. 京都大学プレスリリース. 2011-06-09.
Rights: © 2011 Nature Publishing Group
This is not the published version. Please cite only the published version.
DOI(Published Version): 10.1038/nature10106
PubMed ID: 21654807
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