Render Target: STATIC
Render Timestamp: 2024-11-12T10:19:31.038Z
Commit: 3c1f305a63297e594ac8d7bb5424007d592d68be
XML generation date: 2024-09-20 06:15:52.472
Product last modified at: 2024-11-11T09:30:11.905Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

DLL4 Antibody #2589

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 75-80
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50

    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

    DLL4 Antibody detects endogenous levels of total DLL4 protein.

    Species Reactivity:

    Human

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to a region surrounding residue Leu617 of human DLL4. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    Notch signaling is activated upon engagement of the Notch receptor with its ligands, the DSL (Delta, Serrate, Lag2) proteins of single-pass type I membrane proteins. The DSL proteins contain multiple EGF-like repeats and a DSL domain that is required for binding to Notch (1,2). Five DSL proteins have been identified in mammals: Jagged1, Jagged2, Delta-like (DLL) 1, 3 and 4 (3). Ligand binding to the Notch receptor results in two sequential proteolytic cleavages of the receptor by the ADAM protease and the γ-secretase complex. The intracellular domain of Notch is released and then translocates to the nucleus where it activates transcription. Notch ligands may also be processed in a way similar to Notch, suggesting a bi-directional signaling through receptor-ligand interactions (4-6).
    DLL4 expression is highly restricted to the vascular endothelium (7), and haploinsufficiency of DLL4 results in major defects in vascular systems in mouse (8-11). Blockade of DLL4 inhibits tumor growth in model systems (12-14).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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