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结直肠癌中β-连环蛋白调控的缺陷。

Defects in the regulation of beta-catenin in colorectal cancer.

作者信息

Polakis P, Hart M, Rubinfeld B

机构信息

Onyx Pharmaceuticals, Richmond, California 94806, USA.

出版信息

Adv Exp Med Biol. 1999;470:23-32. doi: 10.1007/978-1-4615-4149-3_3.

Abstract

The molecular events that contribute to the progression of colon cancer are beginning to unravel. An initiating and probably obligatory event is the oncogenic activation of beta-catenin. This can come about by the loss of its negative regulator the adenomatous polyposis coli (APC) protein, or by mutations in the beta-catenin gene that result in a more stable protein product. The interaction between APC and beta-catenin, and additional proteins that affect assembly and signaling along this pathway, are discussed.

摘要

导致结肠癌进展的分子事件正逐渐被揭示。一个起始且可能是必要的事件是β-连环蛋白的致癌激活。这可能通过其负调节因子腺瘤性息肉病大肠杆菌(APC)蛋白的缺失,或通过β-连环蛋白基因中的突变导致更稳定的蛋白质产物而发生。本文讨论了APC与β-连环蛋白之间的相互作用,以及影响该途径组装和信号传导的其他蛋白质。

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