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首页> 外文期刊>The EMBO journal. >CDK1‐mediated BCL9 phosphorylation inhibits clathrin to promote mitotic Wnt signalling
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CDK1‐mediated BCL9 phosphorylation inhibits clathrin to promote mitotic Wnt signalling

机译：CDK1 BCL9磷酸化介导的抑制网格蛋白促进有丝分裂Wnt信号

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摘要

Uncontrolled cell division is a hallmark of cancer. Deregulation of Wnt components has been linked to aberrant cell division by multiple mechanisms, including Wnt‐mediated stabilisation of proteins signalling, which was notably observed in mitosis. Analysis of Wnt components revealed an unexpected role of B‐cell CLL/lymphoma 9 (BCL9) in maintaining mitotic Wnt signalling to promote precise cell division and growth of cancer cell. Mitotic interactome analysis revealed a mechanistic role of BCL9 in inhibiting clathrin‐mediated degradation of LRP6 signalosome components by interacting with clathrin and the components in Wnt destruction complex; this function was further controlled by CDK1‐driven phosphorylation of BCL9?N‐terminal, especially T172. Interestingly, T172 phosphorylation was correlated with cancer patient prognosis and enriched in tumours. Thus, our results revealed a novel role of BCL9 in controlling mitotic Wnt signalling to promote cell division and growth.
机译：不受控制的细胞分裂的一个特点癌症。与多个异常的细胞分裂机制,包括Wnt介导的稳定蛋白质的信号,这是值得注意的观察有丝分裂。揭示了一个意想不到的角色B细胞慢性淋巴细胞白血病/淋巴瘤9 (BCL9)在维护有丝分裂Wnt信号促进精确的细胞分裂和癌细胞的增长。分析显示BCL9的机械作用抑制网格蛋白介导LRP6退化signalosome组件相互作用网格蛋白在Wnt和组件的破坏复杂;CDK1量驱动的磷酸化BCL9吗?尤其是T172。磷酸化是与癌症有关肿瘤患者预后和丰富。我们的研究结果揭示了小说BCL9的角色控制Wnt信号促进有丝分裂细胞分裂和生长。

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