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MAT1-Modulated CAK Activity Regulates Cell Cycle G1 Exit

机译：MAT1调节的CAK活性调节细胞周期G1退出

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The cyclin-dependent kinase (CDK)-activating kinase (CAK) is involved in cell cycle control, transcription, and DNA repair (E. A. Nigg, Curr. Opin. Cell. Biol. 8:312–317, 1996). However, the mechanisms of how CAK is integrated into these signaling pathways remain unknown. We previously demonstrated that abrogation of MAT1 (ménage à trois 1), an assembly factor and targeting subunit of CAK, induces G1 arrest (L. Wu, P. Chen, J. J. Hwang, L. W. Barsky, K. I. Weinberg, A. Jong, and V. A. Starnes, J. Biol. Chem. 274:5564–5572, 1999). This result led us to investigate how deregulation of CAK by MAT1 abrogation affects the cell cycle G1 exit, a process that is regulated most closely by phosphorylation of retinoblastoma tumor suppressor protein (pRb). Using mammalian cellular models that undergo G1arrest evoked by antisense MAT1 abrogation, we found that deregulation of CAK inhibits pRb phosphorylation and cyclin E expression, CAK phosphorylation of pRb is MAT1 dose dependent but cyclin D1/CDK4 independent, and MAT1 interacts with pRb. These results suggest that CAK is involved in the regulation of cell cycle G1 exit while MAT1-modulated CAK formation and CAK phosphorylation of pRb may determine the cell cycle specificity of CAK in G1progression.
机译：细胞周期蛋白依赖性激酶（CDK）激活激酶（CAK）参与细胞周期控制，转录和DNA修复（E. A. Nigg，Curr。Opin。Cell。Biol。8：312-317，1996）。但是，如何将CAK整合到这些信号通路中的机制仍然未知。我们先前证明，废除MAT1（ménageàtrois 1），CAK的装配因子和靶向亚基会诱导G 1 逮捕（L. Wu，P。Chen，JJ Hwang，LW Barsky，KI Weinberg，A。Jong和VA Starnes，J。Biol。Chem。274：5564-5572，1999）。该结果使我们研究了MAT1消除对CAK的放松调节如何影响细胞周期G 1 的退出，这一过程最受视网膜母细胞瘤抑癌蛋白（pRb）磷酸化的调控。使用经历反义MAT1取消引起的G 1 逮捕的哺乳动物细胞模型，我们发现CAK的失调抑制pRb磷酸化和cyclin E的表达，pRb的CAK磷酸化是MAT1剂量依赖性的，而与cyclin D1 / CDK4无关，并且MAT1与pRb相互作用。这些结果提示，CAK参与细胞周期G 1 出口的调控，而MAT1调控的CAK形成和pRb的CAK磷酸化可能决定了CAK在G 1 中的细胞周期特异性。子>进度。

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