Cyclin protein (Cyclin (plural: Cyclins), sometimes abbreviated as CCN (e.g., CCND1 for Cyclin D1), but there is no single universal abbreviation for the entire family)

Cyclins are a large family of regulatory proteins essential for the control of cell cycle progression in eukaryotic cells. They function by binding to and activating cyclin-dependent kinases (CDKs), forming cyclin–CDK complexes that phosphorylate substrates involved in key cell cycle transitions such as DNA replication (S phase) and mitosis (M phase).[1][2][6] Different cyclins are expressed at specific cell cycle stages, driving orderly progression through G1, S, G2, and M phases.[1][2][3][6] Cyclins are structurally defined by a conserved “cyclin box” domain but are otherwise diverse in sequence. Dysregulation of cyclin expression or function is implicated in uncontrolled proliferation and tumorigenesis, making them important in cancer biology and therapy.[1][2][3] Cyclins themselves are not enzymes; their main function is as regulatory subunits that specify CDK activity, subcellular localization, and substrate selection. Most drugs target the CDK partners, but cyclin expression levels are employed as cancer biomarkers and sometimes therapeutic targets (e.g., by inhibiting cyclin D partner CDK4/6 in breast cancer)[1][3].

Other names

Cyclin familyCCN protein familycell cycle cyclinssometimes referred to by individual type (e.g., G1 cyclin, S-phase cyclin, M-phase cyclin)

Inhibition of cyclin–CDK complexes (especially cyclin D–CDK4/6, cyclin E–CDK2, cyclin A–CDK2, cyclin B–CDK1), mainly by blocking CDK activity required for cell cycle progression