1[1]Nurse P. Along twentieth century of the cell cycle and beyond. Cell, 2000, 100: 71~78
2[2]Lundberg A S, Weinberg R A. Functional inactivation of the retinoblastoma protein requires sequential modification by at least two distinct cyclin-cdk complexes. Mol Cell Biol, 1998, 18: 753~761
3[3]Flemington E K, Speck S H, Kaelin W J. E2F-1-mediated transactivation is inhibited by complex formation with the retinoblastoma susceptibility gene product. Proc Natl Acad Sci USA, 1993, 90: 6914~6918
4[4]Harbour J W, Luo R X, Dei Sante A, et al. Cdk phosphorylation triggers sequential intramolecular interaction that progressively block Rb functions as cells move through G1. Cell, 1999, 98: 859~869
5[5]Nguyen V Q, Co C, Li J J. Cyclin-dependent kinases prevent DNA re-replication through multiple mechanisms. Nature, 2001, 411: 1068~1073
6[6]Morgan D O. Cyclin-dependent kinases: engines, clocks, and microprocessors. Annu Rev Cell Dev Biol, 1997, 13: 261~291
7[7]Jeffrey P D, Russo A A, Polyak K, et al. Mechanism of CDK activation revealed by the structure of a cyclin A-CDK2 complex. Nature, 1995, 376: 313~320
8[8]Roberts J M. Evolving ideas about cyclins. Cell, 1999, 98: 129~132
9[9]Sherr C J, Roberts J M. CDK inhibitors: positive and negative regulators of G1-phase progression. Genes Dev, 1999, 13: 1501~1512
10[10]Jeoung D I, Oehlen L J, Cross F R. Cln3-associated kinase activity in Saccharomyc cerevisiae is regulated by the mating factor pathway. Mol Cell Biol, 1998, 18: 433~441