Overview:

Cyclin E was first identified by its ability to rescue growth of yeast deficient in G1 Cyclins, indicating a role in G1 or G1/S transitions.  Over-expression of Cyclin E has been observed in a variety of human tumors. Multiple isoforms of Cyclin E are expressed in tumors but not in normal tissues, suggesting a post-transcriptional regulation of Cyclin E.  Cyclin E2 associates with Cdk2 in a functional kinase complex that is inhibited by both p27Kip1 and p21Cip1.  The catalytic activity associated with Cyclin E2 complexes is cell cycle regulated and peaks at the G1/S transition.  Unlike Cyclin E1, which is expressed in most proliferating normal and tumor cells, Cyclin E2 levels were low to undetectable in non-transformed cells and increased significantly in tumor-derived cells.

References:

1. Philipp, G.Y., et al.:Cyclin E ablation in the mouse. Cell 114(4):431-443. Yu, Q., Sicinski, P. (2004) Mammalian cell cycles without Cyclin E-CDK2. Cell Cycle 2003: 3(3); 292-295. 2. Parisi, T., et al.:Cyclins E1 and E2 are required for endoreplication in placental trophoblast giant cells. EMBO J. 2003: 22(18); 4794-4803. 3. Geng, Y., et al.: Expression of Cyclins E1 and E2 during mouse development and in neoplasia. Proc. Natl. Acad. Sci. USA 2001: 98(23); 13138-13143. 4. Berthet, C., et al.: Cdc2-Cyclin E complexes regulate the G1/S phase transition. Nat. Cell Biol. 2005: 7(8); 831-836.