Render Target: STATIC
Render Timestamp: 2024-11-21T14:10:26.581Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-09-30 01:54:12.112
Product last modified at: 2024-11-12T20:30:08.605Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

DNA Ligase IV (D5N5N) Rabbit mAb #14649

Filter:
  • WB

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 100
    Source/Isotype Rabbit IgG
    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, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    DNA Ligase IV (D5N5N) Rabbit mAb recognizes endogenous levels of total DNA ligase IV protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu771 of human DNA ligase IV protein.

    Background

    DNA double-strand breaks (DSBs) are potentially hazardous lesions that can be induced by ionizing radiation (IR), radiomimetic chemicals, or DNA replication inhibitors. Cells detect and repair DSBs through two distinct but partly overlapping signaling pathways, nonhomologous end joining (NHEJ) and homologous recombination (HR). DNA repair through the HR pathway is restricted to S and G2 phases of the cell cycle, while NHEJ can occur during any cell cycle phase. Defects in both pathways have been associated with human disease, including cancer (1).

    DNA repair through the NHEJ pathway involves a core group of proteins that includes the Ku heterodimer, DNA-PKcs, DNA ligase IV, XRCC4, and XLF. XLF interacts with XRCC4 and promotes the ligation of DNA strands by DNA ligase IV and the ligase cofactor XRCC4. The ATP-dependent ligation of free DNA ends is the final step in the NHEJ repair pathway (2). Research studies suggest that XLF and XRCC4 proteins form complexes that bridge DNA breaks earlier in the NHEJ pathway (3). Additional studies indicate that localization of XRCC4 to the nucleus and levels of XRCC4 protein are both regulated by DNA ligase IV (4). Mutations in the corresponding LIG4 gene are associated with LIG4 syndrome, a disorder characterized by immunodeficiency and developmental growth delay. Cells isolated from patients diagnosed with LIG4 syndrome display typical cell cycle checkpoint activity, but aberrant rejoining of DNA double strand breaks (5,6).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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