research use only

Cyclin C Antibody [J7J21]

Cat.No.: F8140

    Application: Reactivity:

    Usage Information

    Dilution
    1:1000
    1:100
    1:1600 - 1:6400
    1:100 - 1:400
    Application
    WB, IP, IF, FCM
    Reactivity
    Human, Mouse
    Source
    Rabbit Monoclonal Antibody
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW
    30 kDa
    Positive Control 293T cells;A-172 cells;A-204 cells;ACHN cells;HCC1806 cells;K-562 cells;NIH/3T3 cells;C2C12 cells;HCT 116 cells
    Negative Control

    Datasheet & SDS

    Biological Description

    Specificity
    Cyclin C Antibody [J7J21] detects endogenous levels of total Cyclin C protein.
    Clone
    J7J21
    Synonym(s)
    Cyclin-C; SRB11 homolog (hSRB11); CCNC
    Background
    Cyclin C is a regulatory subunit of the cyclin family that partners specifically with CDK8 (forming the CDK8/Cyclin C kinase module of the Mediator complex) and CDK3 to control transcription and cell cycle transitions, rather than the canonical G1/S progression. It contains two canonical five-helix repeats that flank a flexible N-terminal α-helix, which is short, mobile, and exposed for non-CDK interactions. This N-terminal helix docks onto CDK8's PSTAIRE helix and αC-helix, inducing the active DFG-in (DMG-in for CDK8) conformation without the need for T-loop phosphorylation. Key interaction hotspots include Glu99 of Cyclin C, which orients CDK8's conserved arginines (R158, R356, R366) and stabilizes the activation loop and αB/αC-helices through hydrogen bonding networks. The Cyclin C/CDK8 complex phosphorylates RNA polymerase II CTD at Ser2 and Ser5, MED13, and transcription factors such as STAT1 and β-catenin to repress super-enhancers, terminate Pol II pause-release, and fine-tune immediate-early gene expression. In response to stress, nuclear export releases Cyclin C to the cytosol, where it activates Drp1 and Bax for mitochondrial outer membrane permeabilization, fission, and apoptosis through synergistic PTEN, p53, and p21 signaling. Cyclin C also regulates thyroid cancer suppression, Rb-quiescence exit via CDK3, and oxidative stress responses. Its dysregulation can drive colorectal and breast cancer through Mediator hijacking, while cytosolic translocation can promote neurodegeneration and disrupt the balance of apoptosis.
    References
    • https://pubmed.ncbi.nlm.nih.gov/15979093/
    • https://pubmed.ncbi.nlm.nih.gov/33523904/

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