大肠腺瘤性息肉病
连环素
结直肠癌
癌症研究
连环蛋白
基因
生物
转录因子
突变体
抑制器
突变
家族性腺瘤性息肉病
抑癌基因
磷酸化
Wnt信号通路
遗传学
癌症
癌变
作者
Patrice J. Morin,Andrew B. Sparks,Vladimír Kořínek,Nick Barker,Hans Clevers,Bert Vogelstein,Kenneth W. Kinzler
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:1997-03-21
卷期号:275 (5307): 1787-1790
被引量:3746
标识
DOI:10.1126/science.275.5307.1787
摘要
Inactivation of the adenomatous polyposis coli ( APC ) tumor suppressor gene initiates colorectal neoplasia. One of the biochemical activities associated with the APC protein is down-regulation of transcriptional activation mediated by β-catenin and T cell transcription factor 4 (Tcf-4). The protein products of mutant APC genes present in colorectal tumors were found to be defective in this activity. Furthermore, colorectal tumors with intact APC genes were found to contain activating mutations of β-catenin that altered functionally significant phosphorylation sites. These results indicate that regulation of β-catenin is critical to APC's tumor suppressive effect and that this regulation can be circumvented by mutations in either APC or β-catenin.
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