Anastasiadis P Z, Moon S Y, Thoreson M A, Mariner D J, Crawford H C, Zheng Y, Reynolds A B
Department of Cell Biology, Vanderbilt University, MCN C-2310, Nashville, Tennessee 37232-2175, USA.
Nat Cell Biol. 2000 Sep;2(9):637-44. doi: 10.1038/35023588.
RhoA organizes actin stress fibres and is necessary for cell transformation by oncogenes such as src and ras. Moreover, RhoA is implicated in cadherin clustering during the formation of adherens junctions. The catenin p120 has also been implicated in cadherin clustering through an unknown mechanism. Here we show that p120 selectively inhibits RhoA activity in vitro and in vivo. RhoA inhibition and the interaction of p120 with cadherins are mutually exclusive, suggesting a mechanism for regulating the recruitment and exchange of RhoA at nascent cell-cell contacts. By affecting RhoA activation, p120 could modulate cadherin functions, including suppression of invasion, neurite extension and junction formation.
RhoA可组织肌动蛋白应激纤维,是src和ras等癌基因诱导细胞转化所必需的。此外,RhoA在黏附连接形成过程中参与钙黏蛋白的聚集。连环蛋白p120也通过未知机制参与钙黏蛋白的聚集。在此我们表明,p120在体外和体内均能选择性抑制RhoA活性。RhoA抑制以及p120与钙黏蛋白的相互作用相互排斥,这提示了一种在新生细胞间接触部位调节RhoA募集和交换的机制。通过影响RhoA激活,p120可调节钙黏蛋白的功能,包括抑制侵袭、神经突延伸和连接形成。