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p27Kip1 is needed...for glioma invasion.

机译：需要p27Kip1 ...用于神经胶质瘤的侵袭。

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摘要

p27kipl (p27) is best known for its role as a negative regulator of cell proliferation via the inhibition of cydin-CDK activities. However, increasing evidence indicates that p27 functions are not limited to cell cycle control but also extend to other cellular processes, including the regulation of cell migration, survival/ apoptosis and genetic instability. Moreover, at least some of these cyclin-CDK independent functions are in fact oncogenic in vivo.The control of cell migration by p27 is mediated via the binding of p27 to the small GTPase RhoA, which prevents the latter from interacting with its activators, the guanine nucleotide exchange factors (GEFs).The RhoA/ p27 interaction is mediated by the C-terminal half of p27 and it appears that phosphoryla-tion of the last residue of p27 (Thr-198) is important for binding. Notably, Thr-198 is also involved in the regulation of p27 stability and in the cytoplasmic retention of p27.
机译：p27kipl（p27）最出名的是它通过抑制cydin-CDK活性作为细胞增殖的负调节剂。但是，越来越多的证据表明p27功能不仅限于细胞周期控制，而且还扩展到其他细胞过程，包括细胞迁移，存活/凋亡和遗传不稳定性的调节。而且，至少这些细胞周期蛋白-CDK独立功能实际上是体内致癌的。p27对细胞迁移的控制是通过p27与小GTPase RhoA的结合来介导的，这阻止了后者与它的激活剂（即Ghoase）相互作用。鸟嘌呤核苷酸交换因子（GEFs）。RhoA/ p27相互作用是由p27的C端一半介导的，看来p27的最后一个残基（Thr-198）的磷酸化对于结合很重要。值得注意的是，Thr-198还参与了p27稳定性的调节和p27的胞质保留。

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