Render Target: SSR
Render Timestamp: 2024-11-23T07:31:13.138Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-09-20 06:17:41.924
Product last modified at: 2024-09-13T07:01:46.743Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

Phospho-CDK4 (Thr172) Antibody #5884

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  • WB

Inquiry Info. # 5884

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    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 30
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    Storage

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

    Protocol

    Specificity / Sensitivity

    Phospho-CDK4 (Thr172) Antibody recognizes endogenous levels of CDK4 protein only when phosphorylated at Thr172.

    Species Reactivity:

    Human

    The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.

    Species predicted to react based on 100% sequence homology:

    Mouse, Rat, Monkey, Dog, Pig

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Thr172 of human CDK4 protein. Antibodies are purified by protein A and peptide affinity chromatography.

    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).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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