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冯·希佩尔-林道肿瘤抑制蛋白通过驱动蛋白-2与微管相互作用。

The von Hippel-Lindau tumour suppressor interacts with microtubules through kinesin-2.

作者信息

Lolkema Martijn P, Mans Dorus A, Snijckers Cristel M, van Noort Mascha, van Beest Moniek, Voest Emile E, Giles Rachel H

机构信息

Department of Medical Oncology, University Medical Center Utrecht, Heidelberglaan 100, rm F02.126, 3584 CX Utrecht, The Netherlands.

出版信息

FEBS Lett. 2007 Oct 2;581(24):4571-6. doi: 10.1016/j.febslet.2007.08.050. Epub 2007 Aug 31.

Abstract

Synthesis and maintenance of primary cilia are regulated by the von Hippel-Lindau (VHL) tumour suppressor protein. Recent studies indicate that this regulation is linked to microtubule-dependent functions of pVHL such as orienting microtubule growth and increasing plus-end microtubule stability, however little is known how this occurs. We have identified the kinesin-2 motor complex, known to regulate cilia, as a novel and endogenous pVHL binding partner. The interaction with kinesin-2 facilitates pVHL binding to microtubules. These data suggest that microtubule-dependent functions of pVHL are influenced by kinesin-2.

摘要

原发性纤毛的合成与维持受冯·希佩尔-林道(VHL)肿瘤抑制蛋白调控。最近的研究表明,这种调控与磷酸化VHL(pVHL)的微管依赖性功能相关,比如引导微管生长以及增强微管正端稳定性,然而对于其具体发生机制却知之甚少。我们已确定驱动蛋白-2运动复合体(已知其可调控纤毛)是一种新的内源性pVHL结合伴侣。与驱动蛋白-2的相互作用促进pVHL与微管结合。这些数据表明,pVHL的微管依赖性功能受驱动蛋白-2影响。

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