Non-proteolytic inactivation of geminin requires CDK-dependent ubiquitination.

Non-proteolytic inactivation of geminin requires CDK-dependent ubiquitination.
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DOI:
10.1038/ncb1100
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发表时间:
2004-03
影响因子:
21.3
通讯作者:
Blow, JJ
Blow, JJ
中科院分区:
生物学1区
文献类型:
--
作者:
Li, A;Blow, JJ

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在有丝分裂晚期和G1期,Mcm2-7被组装到复制起点上,“许可”它们开始。在其他时候,细胞周期蛋白依赖激酶(CDKs)和双联蛋白抑制了许可,从而确保每个细胞周期只激活一次起源。我们在这里表明,自相矛盾的是,cdk也需要灭活双胞蛋白和激活许可系统。在非洲爪蟾卵提取物中,cdk依赖的后期促进复合体(APC/C)的激活导致双胞蛋白的多泛素化。这种泛素化不需要泛素依赖的蛋白水解就能触发双胞蛋白失活,这是复制起始获得许可的必要条件。
In late mitosis and G1, Mcm2-7 are assembled onto replication origins to “license” them for initiation. At other times licensing is inhibited by cyclin dependent kinases (CDKs) and geminin, thus ensuring that origins fire only once per cell cycle. We show here that, paradoxically, CDKs are also required to inactivate geminin and activate the licensing system. On exit from metaphase in Xenopus egg extracts, CDK-dependent activation of the Anaphase Promoting Complex (APC/C) results in the polyubiquitination of geminin. This ubiquitination triggers geminin inactivation without requiring ubiquitin-dependent proteolysis, and is essential for replication origins to become licensed.
DOI: 10.1111/j.1432-1033.1997.t01-2-00527.x
发表时间: 1997-01-15
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