Human LATS1 is a mitotic exit network kinase
Human LATS1 is a mitotic exit network kinase
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DOI：
10.1158/0008-5472.can-05-0862
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发表时间：
2005-08-01
期刊：
影响因子：
11.2
通讯作者：
Halazonetis, TD
中科院分区：
文献类型：
--
作者：
Bothos, J;Tuttle, RL;Halazonetis, TD
LATS/WARTS激酶是一种在进化过程中保守的肿瘤抑制蛋白，但其在分子水平上的功能尚不清楚。我们在这里报道了人类LATS1与MOB1A相互作用，MOB1A是一种蛋白，其在出芽酵母中的同源物与参与有丝分裂退出的激酶相关。这表明，在高等真核生物中，LATS1可能是先前未被表征的有丝分裂退出网络的一个组成部分。事实上，暴露于微管毒物的细胞中，人类LATS1的适度过表达促进了有丝分裂的退出，而这种活性需要MOB1A。相反，小干扰rna介导的LATS1或MOB1A抑制延长了末期，但对有丝分裂早期阶段的长度没有影响。LATS1在有丝分裂退出中的作用可以解释其先前描述的诱导G(2)阻滞和促进细胞分裂的能力。
The kinase LATS/WARTS is a tumor suppressor protein conserved in evolution, but its function at the molecular level is not well understood. We report here that human LATS1 interacts with MOB1A, a protein whose homologue in budding yeast associates with kinases involved in mitotic exit. This suggested that LATS1 may be a component of the previously uncharacterized mitotic exit network in higher eukaryotes. Indeed, moderate overexpression of human LATS1 in cells exposed to microtubule poisons facilitated mitotic exit, and this activity required MOB1A. Reciprocally, small interfering RNA-mediated suppression of LATS1 or MOB1A prolonged telophase, but had no effect on the length of the earlier phases of mitosis. A role of LATS1 in mitotic exit may explain its previously described abilities to induce G(2) arrest and promote cytokinesis.