| First Author | Möröy T | Year | 2004 |
| Journal | Int J Biochem Cell Biol | Volume | 36 |
| Issue | 8 | Pages | 1424-39 |
| PubMed ID | 15147722 | Mgi Jnum | J:90143 |
| Mgi Id | MGI:3042623 | Doi | 10.1016/j.biocel.2003.12.005 |
| Citation | Moroy T, et al. (2004) Cyclin E. Int J Biochem Cell Biol 36(8):1424-1439 |
| abstractText | E-type cyclins (cyclin E1 and cyclin E2) are expressed during the late G1 phase of the cell cycle until the end of the S-phase. The activity of cyclin E is limiting for the passage of cells through the restriction point 'R' which marks a 'point of no return' for cells entering the division cycle from a resting state or passing from G1 into S-phase. Expression of cyclin E is regulated on the level of gene transcription mainly by members of the E2F trrnscription factor family and by its degradation via the proteasome pathway. Cyclin E binds and activates the kinase Cdk2 and by phosphorylating its substrates, the so-called 'pocket proteins', the cyclic/Cdk2 complexes initiate a cascade of events that leads to the expression of S-phase specific genes. Aside from this specific function as a regulator of S-phase-entry, cyclin E plays a direct role in the initiation of DNA replication, the control of genomic stability, and the centrosome cycle. Surprisingly, recent studies have shown that the once thought essential cyclin E is dispensable for the development of higher eukaryotes and for the mitotic division of eukaryotic cells. Nevertheless, high level cyclin E expression has been associated with the initiation or progression of different human cancers, in particular breast cancer but also leukemia, lymphoma and others. Transgenic mouse models in which cyclin E is constitutively expressed develop malignant diseases, supporting the notion of cyclin E as a dominant onco-protein. |
