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首页> 外文期刊>Cell motility and the cytoskeleton >Phosphorylation of MAP2c and MAP4 by MARK kinases leads to the destabilization of microtubules in cells.
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Phosphorylation of MAP2c and MAP4 by MARK kinases leads to the destabilization of microtubules in cells.

机译：MARK激酶使MAP2c和MAP4磷酸化会导致细胞中微管的不稳定。

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摘要

Microtubules serve as transport tracks in molecular mechanisms governing cellular shape and polarity. Rapid transitions between stable and dynamic microtubules are regulated by several factors, including microtubule-associated proteins (MAPs). We have shown that MAP/microtubule affinity regulating kinases (MARK) can phosphorylate the microtubule-associated-proteins MAP4, MAP2c, and tau on their microtubule-binding domain in vitro. This leads to their detachment from microtubules (MT) and an increased dynamic instability of MT. Here we show that MARK protein kinases phosphorylate MAP2 and MAP4 on their microtubule-binding domain in transfected CHO cells. In CHO cells expressing MARK1 or MARK2 under control of an inducible promoter, MARK2 phosphorylates an endogenous MAP4-related protein. Prolonged expression of MARK2 results in microtubule-disruption, detachment of cells from the substratum, and cell death. Concomitant with microtubule disruption, we also observed a breakdown of the vimentin network, whereas actin fibers remained unaffected. Thus, MARK seems to play an important role in controlling cytoskeletal dynamics. Copyright 1999 Wiley-Liss, Inc.
机译：微管在控制细胞形状和极性的分子机制中充当转运通道。稳定和动态微管之间的快速转换受多种因素调节，包括微管相关蛋白（MAPs）。我们已经表明，MAP /微管亲和力调节激酶（MARK）可以在其微管结合域上磷酸化微管相关蛋白MAP4，MAP2c和tau。这导致它们从微管（MT）脱离，并增加了MT的动态不稳定性。在这里，我们显示了MARK蛋白激酶在转染的CHO细胞中的微管结合域上磷酸化了MAP2和MAP4。在可诱导的启动子控制下表达MARK1或MARK2的CHO细胞中，MARK2磷酸化内源性MAP4相关蛋白。 MARK2的延长表达会导致微管破裂，细胞从基底脱离以及细胞死亡。与微管破裂，我们还观察到波形蛋白网络的崩溃，而肌动蛋白纤维仍然不受影响。因此，MARK似乎在控制细胞骨架动力学中起重要作用。版权所有1999 Wiley-Liss，Inc.

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