Nakano Naoko, Kato Mitsuyasu, Itoh Susumu
Laboratory of Biochemistry, Showa Pharmaceutical University, 3-3165 Higashi-Tamagawagakuen, Machida, Tokyo 194-8543, Japan; Laboratory of Experimental Pathology, Graduate School of Comprehensive Human Sciences and Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8577, Japan.
Laboratory of Experimental Pathology, Graduate School of Comprehensive Human Sciences and Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8577, Japan.
J Biochem. 2016 Jan;159(1):27-30. doi: 10.1093/jb/mvv117. Epub 2015 Nov 20.
We previously found that TCF7L2 could activate the TMEPAI gene efficiently, whereas LEF1 could not nearly augment its transcription. When we comprehended the functional difference(s) between TCF7L2 and LEF1 with respect to the activation of the TMEPAI gene, the C-terminal tail of TCF7L2 was needed to reveal its transcriptional activity as well as its interaction with Smad3. Consistently, both TCF7/TCF7L2 and LEF1/TCF7L2 chimeric proteins exhibited an activity similar to TCF7L2 in transcription and Smad3 binding in contrast with LEF1 and TCF7. Our data elaborated on the diverse activity among TCF/LEF family members with respect to the transcriptional regulation of the TMEPAI gene.
我们先前发现，TCF7L2能够有效地激活TMEPAI基因，而LEF1几乎不能增强其转录。当我们了解TCF7L2和LEF1在激活TMEPAI基因方面的功能差异时，需要TCF7L2的C末端尾巴来揭示其转录活性以及它与Smad3的相互作用。一致的是，与LEF1和TCF7相比，TCF7/TCF7L2和LEF1/TCF7L2嵌合蛋白在转录和Smad3结合方面均表现出与TCF7L2相似的活性。我们的数据阐述了TCF/LEF家族成员在TMEPAI基因转录调控方面的不同活性。
