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On the move: p27(Kip1) drives cell motility in glioma cells.

机译:在移动中:p27(Kip1)驱动神经胶质瘤细胞的细胞运动。

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摘要

Cells from metastatic or invasive tumors require the ability to become motile and degrade the extracellular matrix and basement membranes, which are stabilized by actin stress fibers when producing tension across the cell, allowing the cell to pull and anchor on to a substrate (e.g., the extracellular matrix). Actin stress fibers are stabilized by Rho GTPases that switch between inactive GDP-bound and active GTP-bound states. Specifically, RhoA bound to GDP is activated by guanine-nucleotide exchange factors (GEFs). GTP-bound RhoA activates a signaling cascade leading to phosphorylation of cofilin, an actin-depolymerizing protein. This phosphorylation inhibits cofilin activity, resulting in stabilization of actin filaments.
机译:来自转移性或侵袭性肿瘤的细胞需要能够移动并降解细胞外基质和基底膜的能力,当跨细胞产生张力时,肌动蛋白应激纤维会稳定这些细胞外基质和基底膜,从而使细胞能够拉动并锚定在基质上(例如,细胞外基质)。肌动蛋白应力纤维由Rho GTPases稳定,Rho GTPases在无效GDP约束状态和有效GTP约束状态之间切换。具体而言,与GDP结合的RhoA被鸟嘌呤-核苷酸交换因子(GEF)激活。 GTP结合的RhoA激活信号级联反应,导致肌动蛋白解聚蛋白cofilin磷酸化。这种磷酸化抑制了cofilin活性,导致肌动蛋白丝的稳定性。

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