Suppr超能文献

TCF/LEF因子崭露头角。

TCF/LEF factor earn their wings.

作者信息

Clevers H, van de Wetering M

机构信息

Department of Immunology, University Hospital Utrecht, The Netherlands.

出版信息

Trends Genet. 1997 Dec;13(12):485-9. doi: 10.1016/s0168-9525(97)01305-x.

Abstract

Factors of the TCF/LEF HMG domain family (TCFs) exist in vertebrates, Drosophila melanogaster and Caenorhabditis elegans. It has very recently become evident that TCFs interact with the vertebrate WNT effector beta-catenin to mediate axis formation in Xenopus. Likewise, Armadillo (the Drosophila ortholog of beta-catenin) is genetically upstream of a Drosophila TCF in the Wingless pathway. Upon Wingless/Wnt signaling, Armadillo/beta-catenin associate with nuclear TCFs and contribute a trans-activation domain to the resulting bipartite transcription factor. The cytoplasmic tumor-suppressor protein APC binds to beta-catenin causing its destruction. In APC-deficient colon carcinoma cells, beta-catenin accumulates and is constitutively complexed with TCF factors. In APC-positive colon carcinomas and melanomas, dominant mutations in beta-catenin render it indestructable, providing an alternative mechanism to activate transcription of TCF target genes inappropriately. So, transcriptional activation of TCF target genes by beta-catenin appears to be a central event in development and cellular transformation.

摘要

TCF/LEF HMG结构域家族(TCFs)的因子存在于脊椎动物、黑腹果蝇和秀丽隐杆线虫中。最近很明显的是,TCFs与脊椎动物WNT效应因子β-连环蛋白相互作用,以介导非洲爪蟾的轴形成。同样,犰狳(β-连环蛋白的果蝇直系同源物)在无翅通路中位于果蝇TCF的遗传上游。在无翅/Wnt信号传导时,犰狳/β-连环蛋白与核TCFs结合,并为产生的二分体转录因子贡献一个反式激活结构域。细胞质肿瘤抑制蛋白APC与β-连环蛋白结合导致其降解。在APC缺陷的结肠癌细胞中,β-连环蛋白积累并与TCF因子持续形成复合物。在APC阳性的结肠癌和黑色素瘤中,β-连环蛋白的显性突变使其无法降解,提供了一种不适当激活TCF靶基因转录的替代机制。因此,β-连环蛋白对TCF靶基因的转录激活似乎是发育和细胞转化中的一个核心事件。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验