Render Target: STATIC
Render Timestamp: 2024-12-16T13:27:37.150Z
Commit: 611277b6de3cd1bb065350b6ef8d63df412b7185
XML generation date: 2024-04-05 20:28:13.413
Product last modified at: 2024-05-30T07:10:07.801Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77

CDK4 (DCS156) Mouse mAb #2906

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Inquiry Info. # 2906

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    Supporting Data

    REACTIVITY H M
    SENSITIVITY Endogenous
    MW (kDa) 30
    Source/Isotype Mouse IgG1
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:2000

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    CDK4 (DCS156) Mouse mAb detects endogenous levels of total CDK4 protein. The antibody does not cross-react with other CDKs.

    Species Reactivity:

    Human, Mouse

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with recombinant human CDK4 corresponding to amino acids 270-290.

    Background

    Cyclin-dependent kinase activity is regulated by T-loop phosphorylation (Thr172 in the case of CDK4), by the abundance of their cyclin partners, and by association with CDK inhibitors of the Cip/Kip or INK family of proteins (1). The inactive ternary complex of CDK4/cyclin D and p27 Kip1/Cip1 requires extracellular mitogenic stimuli for the release and degradation of p27, which affects progression through the restriction point and pRb-dependent entry into S-phase (2). The active complex of CDK4/cyclin D targets the retinoblastoma protein for phosphorylation, allowing the release of E2F transcription factors that activate G1/S-phase gene expression (3). In HeLa cells, upon UV irradiation, upregulation of p16 INK4A association with CDK4/cyclin D3 leads to a G2 delay, implicating CDK4/cyclin D3 activity in progression through the G2-phase of the cell cycle (4).
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