Human cyclin E, originally identified on the basis of its ability to function as a G1 cyclin in budding yeast, associated with a cell cycle-regulated protein kinase in human cells. The cyclin E-associated kinase activity peaked during G1, before the appearance of cyclin A, and was diminished during exit from the cell cycle after differentiation or serum withdrawal. The major cyclin E-associated kinase in human cells was Cdk2 (cyclin-dependent kinase 2). The abundance of the cyclin E protein and the cyclin E-Cdk2 complex was maximal in G1 cells. These results provide further evidence that in all eukaryotes assembly of a cyclin-Cdk complex is an important step in the biochemical pathway that controls cell proliferation during G1.

Koff, A., Giordano, A., Desai, D., Yamashita, K., Harper, J.W., Elledge, S., et al. (1992). Formation and activation of a cyclin E-cdk2 complex during the G1 phase of the human cell cycle. SCIENCE, 257(5077), 1689-1694 [10.1126/science.1388288].

Formation and activation of a cyclin E-cdk2 complex during the G1 phase of the human cell cycle

Giordano, A.;
1992-01-01

Abstract

Human cyclin E, originally identified on the basis of its ability to function as a G1 cyclin in budding yeast, associated with a cell cycle-regulated protein kinase in human cells. The cyclin E-associated kinase activity peaked during G1, before the appearance of cyclin A, and was diminished during exit from the cell cycle after differentiation or serum withdrawal. The major cyclin E-associated kinase in human cells was Cdk2 (cyclin-dependent kinase 2). The abundance of the cyclin E protein and the cyclin E-Cdk2 complex was maximal in G1 cells. These results provide further evidence that in all eukaryotes assembly of a cyclin-Cdk complex is an important step in the biochemical pathway that controls cell proliferation during G1.
1992
Koff, A., Giordano, A., Desai, D., Yamashita, K., Harper, J.W., Elledge, S., et al. (1992). Formation and activation of a cyclin E-cdk2 complex during the G1 phase of the human cell cycle. SCIENCE, 257(5077), 1689-1694 [10.1126/science.1388288].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/38473
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