Target intelligence / Profile preview

Cyclin C (CCNC)

Target
CCNC
Molecular classification
Cyclin, Transcription cofactor, Cell cycle regulatory protein
01

Overview

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].

Other names
Cyclin-CCCNChSRB11CycCSRB11 homologSRB11
02

Mechanism of action

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

03

Biological functions

Regulation of transcriptionCell cycle progression (especially G0-G1 transition)Tumor suppressionModulation of mitochondrial dynamics (response to oxidative stress, apoptosis induction)
04

Disease associations

Cancer (notably T-cell acute lymphoblastic leukemia and other malignancies)Retinal macular dystrophyPotential other proliferative and degenerative diseases
05

Safety considerations

Potential risk of impaired cell cycle regulation or transcriptional dysregulation if inhibitedPossible effects on apoptosis and mitochondrial stability

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