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在HeLa细胞中,将肌球蛋白-I myr 3靶向至由显性活性Cdc42诱导形成的细胞间黏附连接。

Targeting of the myosin-I myr 3 to intercellular adherens type junctions induced by dominant active Cdc42 in HeLa cells.

作者信息

Stöffler H E, Honnert U, Bauer C A, Höfer D, Schwarz H, Müller R T, Drenckhahn D, Bähler M

机构信息

Adolf-Butenandt-Institute, Cell Biology, Ludwig-Maximilians-University, D-80336 Munich, Germany.

出版信息

J Cell Sci. 1998 Sep;111 ( Pt 18):2779-88. doi: 10.1242/jcs.111.18.2779.

DOI:10.1242/jcs.111.18.2779
PMID:9718370
Abstract

Myr 3, a member of the myosin-I family from rat, is shown in this study to be localized at adherens-type intercellular junctions in epithelial and nonepithelial tissues. Formation of intercellular junctions and the accompanying recruitment of myr 3 to these junctions involves signaling by the Rho subfamily of small GTP-binding proteins. This conclusion is based on studies with HtTA-1 HeLa cells that were induced by overexpression of constitutively active Cdc42Hs to form typical adherens-type intercellular junctions enriched in cadherins (N-cadherin), beta-catenin, filamentous actin and myr 3. Recruitement of myr 3 to Cdc42-induced adherens junctions in HeLa cells was dependent on a short region of the tail domain and a functional myosin motor domain, but was independent of its myosin-I tail homology and SH3 regions. Overexpression of constitutively active Rac1 induced a distinct type of adherens junction in HeLa cells that was characterized by elaborate intercellular interdigitations enriched in N-cadherin, beta-catenin and F-actin. Myr 3 was often present, but not specifically enriched in the intercellular junctions induced by constitutively active Rac1.

摘要

Myr 3是一种来自大鼠的肌球蛋白-I家族成员,本研究表明其定位于上皮组织和非上皮组织中的黏附型细胞间连接。细胞间连接的形成以及随之而来的Myr 3向这些连接的募集涉及小GTP结合蛋白Rho亚家族的信号传导。这一结论基于对HtTA-1 HeLa细胞的研究,这些细胞通过组成型活性Cdc42Hs的过表达被诱导形成富含钙黏着蛋白(N-钙黏着蛋白)、β-连环蛋白、丝状肌动蛋白和Myr 3的典型黏附型细胞间连接。Myr 3向HeLa细胞中Cdc42诱导的黏附连接的募集依赖于尾部结构域的一个短区域和一个功能性肌球蛋白运动结构域,但不依赖于其肌球蛋白-I尾部同源性和SH3区域。组成型活性Rac1的过表达在HeLa细胞中诱导了一种不同类型的黏附连接,其特征是富含N-钙黏着蛋白、β-连环蛋白和F-肌动蛋白的精细细胞间指状交叉。Myr 3经常存在,但在组成型活性Rac1诱导的细胞间连接中没有特异性富集。

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