Bau, a splice form of Neurabin-I that interacts with the tumor suppressor Bin1, inhibits malignant cell transformation.

J Duhadaway, F Rowe, K Elliott, N C Mao, G C Prendergast
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引用次数: 5

Abstract

Bin1 is a nucleocytoplasmic adaptor protein and tumor suppressor. A novel protein termed Bau was identified through its ability to interact with a region of Bin1 required to inhibit malignant cell transformation by certain oncogenes. Bau is a splice form of Neurabin-I, one of two related F-actin-binding proteins that are proposed to link cadherin-based cell-cell adhesion sites with the growth regulatory kinase p70S6K. Bau lacks actin- and p70S6K-binding domains found in Neurabin-I but includes coiled-coil domains that are part of its central domain as well as additional sequences not found in Neurabin-I. Interaction with Bin1 requires the presence of the U3 region which is alternately spliced in muscle cells. Bau localizes to the nucleus and cytosol. Like Bin1, Bau can suppress oncogene-mediated transformation and inhibit tumor cell growth. We suggest that Bau may link Bin1 to the Neurabin-I/p70S6K system in muscle and other cells, perhaps providing a mechanism to influence adhesion-dependent signals which affect cell fate.

Bau是neurabin - 1的一种剪接形式,与肿瘤抑制因子Bin1相互作用,抑制恶性细胞转化。
Bin1是一种核细胞质接头蛋白和肿瘤抑制蛋白。一种名为Bau的新蛋白通过其与Bin1区域相互作用的能力被鉴定出来,该区域是抑制某些癌基因的恶性细胞转化所必需的。Bau是neurabin - 1的一种剪接形式,neurabin - 1是两种相关的f -actin结合蛋白之一,被提出将钙粘蛋白为基础的细胞-细胞粘附位点与生长调节激酶p70S6K连接起来。Bau缺乏在Neurabin-I中发现的actin-和p70s6k结合结构域,但包括作为其中心结构域一部分的卷曲结构域以及在Neurabin-I中未发现的其他序列。与Bin1的相互作用需要在肌肉细胞中交替剪接的U3区域的存在。Bau定位于细胞核和细胞质。与Bin1一样,Bau可以抑制癌基因介导的转化,抑制肿瘤细胞的生长。我们认为Bau可能将Bin1与肌肉和其他细胞中的Neurabin-I/p70S6K系统联系起来,可能提供一种机制来影响影响细胞命运的粘附依赖性信号。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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