SOX9 is an intestine crypt transcription factor, is regulated by the Wnt pathway, and represses the CDX2 and MUC2 genes.
SOX9 is an intestine crypt transcription factor, is regulated by the Wnt pathway, and represses the CDX2 and MUC2 genes.
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DOI：
10.1083/jcb.200311021
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发表时间：
2004-07-05
期刊：
影响因子：
--
通讯作者：
Jay P
中科院分区：
文献类型：
--
作者：
Blache P;van de Wetering M;Duluc I;Domon C;Berta P;Freund JN;Clevers H;Jay P
TCF和SOX蛋白属于高迁移率族盒转录因子家族。而TCFs，Wnt通路的转录效应子，已被广泛牵连在肠上皮的发育，稳态和疾病，对SOX蛋白在该组织中的功能知之甚少。在这里，我们在小鼠胎儿肠道中的SOX表达筛选中鉴定了SOX 9。我们报告说，SOX 9蛋白在肠上皮中表达的Wnt目标的模式特征。我们提供了体外和体内的证据，证明一个双向β-catenin/TCF 4转录因子，Wnt信号通路的效应子，是上皮细胞中SOX 9表达所必需的。最后，在结肠上皮来源的细胞中，SOX 9转录抑制CDX 2和MUC 2基因，通常在肠上皮的成熟绒毛细胞中表达，因此可能有助于祖细胞表型的Wnt依赖性维持。
TCF and SOX proteins belong to the high mobility group box transcription factor family. Whereas TCFs, the transcriptional effectors of the Wnt pathway, have been widely implicated in the development, homeostasis and disease of the intestine epithelium, little is known about the function of the SOX proteins in this tissue. Here, we identified SOX9 in a SOX expression screening in the mouse fetal intestine. We report that the SOX9 protein is expressed in the intestinal epithelium in a pattern characteristic of Wnt targets. We provide in vitro and in vivo evidence that a bipartite β-catenin/TCF4 transcription factor, the effector of the Wnt signaling pathway, is required for SOX9 expression in epithelial cells. Finally, in colon epithelium-derived cells, SOX9 transcriptionally represses the CDX2 and MUC2 genes, normally expressed in the mature villus cells of the intestinal epithelium, and may therefore contribute to the Wnt-dependent maintenance of a progenitor cell phenotype.
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DOI：
10.1083/jcb.153.5.1049
发表时间：
2001-05-28
期刊：
The Journal of cell biology
影响因子：
--
作者：
Gottardi CJ;Wong E;Gumbiner BM
通讯作者：
Gumbiner BM
影响因子：
10.5
作者：
Akiyama, H;Chaboissier, MC;de Crombrugghe, B
通讯作者：
de Crombrugghe, B
影响因子：
--
作者：
CHENG, H
通讯作者：
CHENG, H
影响因子：
6
作者：
Hinoi, T;Tani, M;Fearon, ER
通讯作者：
Fearon, ER
影响因子：
2.6
作者：
Ikeya, M;Takada, S
通讯作者：
Takada, S