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首页> 外文期刊>Journal of Cell Science >Lucky 13 - microtubule depolymerisation by kinesin-13 motors
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Lucky 13 - microtubule depolymerisation by kinesin-13 motors

机译:幸运13-通过驱动蛋白13电机进行微管解聚

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摘要

The kinesin-13 class of motors catalyses microtubule depolymerisation by bending tubulins at microtubule ends. Depolymerisation activity is intrinsic to the kinesin-13 motor core but the activity of the core alone is very low compared with that of constructs that also contain a conserved neck sequence. The full-length dimeric motor is an efficient depolymeriser and also diffuses along the microtubule lattice, which helps it to find microtubule ends. Current evidence supports the idea of a generic mechanism for kinesin-13-catalysed depolymerisation. However, the activity of kinesin-13 motors is precisely localised and regulated in vivo to enable a wide range of cellular roles. The proteins are involved in global control of microtubule dynamics. They also localise to mitotic and meiotic spindles, where they contribute to formation and maintenance of spindle bipolarity, chromosomal congression, attachment correction and chromatid separation. In interphase cells, intricate and subtle mechanisms appear to allow kinesin-13 motors to act on specific populations of microtubules. Such carefully controlled localisation and regulation makes these kinesins efficient, multi-tasking molecular motors.
机译:kinesin-13类马达通过弯曲微管末端的微管蛋白来催化微管解聚。解聚活性是驱动蛋白13马达核心所固有的,但是与也包含保守的颈部序列的构建体相比,单独的核心活性非常低。全长二聚体马达是一种有效的解聚剂,并且也沿微管晶格扩散,这有助于其找到微管末端。目前的证据支持驱动蛋白13催化解聚的通用机制的想法。但是,驱动蛋白13电机的活动在体内被精确定位和调节,以实现广泛的细胞作用。这些蛋白质参与了微管动力学的整体控制。它们还定位于有丝分裂和减数分裂纺锤体,在那里它们有助于纺锤体双极性的形成和维持,染色体转化,附着校正和染色单体分离。在相间细胞中,复杂而微妙的机制似乎使kinesin-13马达能够作用于特定的微管种群。这种精心控制的定位和调节使这些驱动蛋白成为高效的多任务分子电动机。

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