Matsushime H
Department of Genetics, University of Tokyo.
Nihon Rinsho. 1995 Apr;53(4):844-9.
Temporally orderly activation of cyclin-dependent kinases (Cdks) governs progression and transitions of the cell cycle in eukaryotic cells. Binding of Cdks to cyclins and threonine phosphorylation in the Cdks are required to form fully active holo-Cdks. So far, 8 types of cyclins and 7 Cdks are known in mammals. Two types of the cyclins, D-(D1, D2, D3) and E-type cyclins, function in the G1 phase of the cell cycle. D-type cyclins form active complexes with Cdk 4 or Cdk 6 earlier than E-type cyclin does with Cdk 2. Overexpression of the cyclin D1 has been reported in human tumors including parathyroid adenomas with chromosomal abnormality, suggesting that overexpression of the cyclin D1 could abrogate cell cycle control in G1 phase and may contribute to generate tumor cells.
细胞周期蛋白依赖性激酶（Cdks）的时间顺序激活控制着真核细胞中细胞周期的进程和转换。Cdk与细胞周期蛋白结合以及Cdk中的苏氨酸磷酸化是形成完全活性的全酶Cdk所必需的。到目前为止，在哺乳动物中已知有8种类型的细胞周期蛋白和7种Cdk。其中两种细胞周期蛋白，即D型（D1、D2、D3）和E型细胞周期蛋白，在细胞周期的G1期发挥作用。D型细胞周期蛋白比E型细胞周期蛋白与Cdk 2更早地形成与Cdk 4或Cdk 6的活性复合物。据报道，细胞周期蛋白D1在包括伴有染色体异常的甲状旁腺腺瘤在内的人类肿瘤中过表达，这表明细胞周期蛋白D1的过表达可能会废除G1期的细胞周期控制，并可能有助于产生肿瘤细胞。
