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亮亮燕燕

Oct4 was a novel target of Wnt signaling pathway.  
7 B! s! b# z9 M, Y) n作者: Li, Jun; Li, Jingyi; Chen, Bingbo
! b$ n- z! _7 @0 n/ }* _. ^: `来源出版物: Molecular and cellular biochemistry  卷: 362   期: 1-2   页: 233-40   出版年: 2012-Mar (Epub 2011 Nov 26)  ! E# b1 j( x: R9 h  r3 b
[ PubMed 相关论文] 3 O$ z" _7 ~* A* W
摘要: The specific expression of Oct4 during early mouse development is required for the correct maintenance of pluripotent cells, and the regulatory control of the Oct4 expression is important. Wnt signaling could have multiple and/or complex effects on embryonic stem (ES) cells characteristics. Elucidation of the molecular mechanisms affecting Wnt signaling in ES cells could provide a better understanding of how these effects occur. The purpose of this study was to determine whether Oct4 was regulated by Wnt signaling in undifferentiated ES cells. Here, we report Oct4 as a novel target of beta-catenin-mediated transcription. First, we observe that Wnt signaling pathway is activated in undifferentiated mouse ES cells. In 239T cells, Oct4 promoter was regulated by beta-catenin. Through promoter mapping and chromatin immuno-precipitation assays, we found that Oct4 is a direct target of beta-catenin/TCF-mediated transcription and the binding site at -875/-881 of Oct4 promoter is critical for b-catenin/TCF-dependent expression regulation. We further detect the expression of Oct4 in treatment with glycogen syntheses kinase (GSK)-3-specific inhibitor in mouse ES cells and HepG2 cells. We found that GSK-3-specific inhibitor can maintain the expression of Oct4 in ES cells and can enhance the expression of Oct4 in HepG2 cells. Our results suggest that Oct4 might be a novel target of beta-catenin/TCF-mediated downstream gene in Wnt-activated cells.  4 w! g: r3 x; z* `5 O# G
PubMed ID: 22120493  " M: q" I" [+ p! @! |0 d
文献类型: Journal Article    @6 U/ y* u2 _& d) M6 p/ M

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