Role of MCM2-7 protein phosphorylation in human cancer cells.
Role of MCM2-7 protein phosphorylation in human cancer cells.
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DOI：
10.1186/s13578-018-0242-2
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发表时间：
2018
影响因子：
7.5
通讯作者：
Xu H
中科院分区：
文献类型：
--
作者：
Fei L;Xu H
由微小染色体维持蛋白2-7（MCM 2 -7）组成的异六聚体复合物是真核生物中关键的复制酶，对于每个细胞周期仅启动一次DNA合成至关重要。MCM复合物在G1期保持无活性，直到S期，此时它被激活以启动复制。在从G1期到S期的过渡期间，MCM经历多位点磷酸化，这是促进其他复制体成员随后组装的重要变化。磷酸化对于MCM活性和功能的调节至关重要。MCMs可以被多种激酶磷酸化，这些磷酸化事件不仅涉及DNA复制，还涉及细胞周期进程和检查点反应。MCMs的功能性磷酸化似乎与癌症的发生和发展相关。本文综述了MCM磷酸化的调控机制和功能后果，并探讨了蛋白激酶抑制剂用于靶向MCM磷酸化治疗癌症的可能性。
A heterohexameric complex composed of minichromosome maintenance protein 2–7 (MCM2–7), which acts as a key replicative enzyme in eukaryotes, is crucial for initiating DNA synthesis only once per cell cycle. The MCM complex remains inactive through the G1 phase, until the S phase, when it is activated to initiate replication. During the transition from the G1 to S phase, the MCM undergoes multisite phosphorylation, an important change that promotes subsequent assembly of other replisome members. Phosphorylation is crucial for the regulation of MCM activity and function. MCMs can be phosphorylated by multiple kinases and these phosphorylation events are involved not only in DNA replication but also cell cycle progression and checkpoint response. Dysfunctional phosphorylation of MCMs appears to correlate with the occurrence and development of cancers. In this review, we summarize the currently available data regarding the regulatory mechanisms and functional consequences of MCM phosphorylation and seek the probability that protein kinase inhibitor can be used therapeutically to target MCM phosphorylation in cancer.
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