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Cyclin C is a highly conserved member of the cyclin family and an essential regulator of both transcription and the cell cycle. It interacts as a regulatory subunit with Cyclin-dependent kinase 8 (CDK8), CDK19, and CDK3, contributing to formation of the CDK8-dependent kinase module within the Mediator complex. This module modulates gene expression by influencing RNA polymerase II–dependent transcription through phosphorylation events. Cyclin C is also implicated in driving cell cycle progression, particularly in the transition from G0 to G1 phase via phosphorylation of retinoblastoma protein when paired with CDK3. Beyond nuclear functions, cyclin C translocates to the cytoplasm in response to oxidative stress, where it directly induces mitochondrial fission and increases cellular sensitivity to apoptosis. Cyclin C acts as a tumor suppressor by regulating pathways such as Notch1. Mutations or dysregulation of CCNC are linked to cancers and retinal degenerative diseases, highlighting its importance in cellular homeostasis, disease, and its potential interest as a therapeutic target[1][2][3][4].
No approved drugs directly targeting cyclin C are listed; mechanisms would include modulation of cyclin C–dependent kinase activity or alteration of transcriptional regulation and cell cycle progression if targeted
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