Synergy between tumor suppressor APC and the β-catenin-Tcf4 target Tcf1

被引：390

作者：

Roose, J

Huls, G

van Beest, M

Moerer, P

van der Horn, K

Goldschmeding, R

Logtenberg, T

Clevers, H

机构：

[1] Univ Utrecht, Med Ctr, Dept Immunol, NL-3508 GA Utrecht, Netherlands

[2] Univ Utrecht, Med Ctr, Ctr Biomed Genet, NL-3508 GA Utrecht, Netherlands

[3] Univ Utrecht, Med Ctr, Dept Pathol, NL-3508 GA Utrecht, Netherlands

来源：

SCIENCE | 1999年 / 285卷 / 5435期

关键词：

D O I：

10.1126/science.285.5435.1923

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Mutations in APC or beta-catenin inappropriately activate the transcription factor Tcf4, thereby transforming intestinal epithelial cells. Here it is shown that one of the target genes of Tcf4 in epithelial cells is Tcf1, The most abundant Tcf1 isoforms Lack a beta-catenin interaction domain. Tcf1(-/-) mice develop adenomas in the gut and mammary glands. Introduction of a mutant APC allele into these mice substantially increases the number of these adenomas. Tcf1 may act as a feedback repressor of beta-catenin-Tcf4 target genes and thus may cooperate with APC to suppress malignant transformation of epithelial cells.

引用

页码：1923 / 1926

页数：4

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