Cell Signaling Technology Logo
1% for the planet logo
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

DLK1 (F7O3Q) Rabbit mAb #94845

Filter:
  • IHC
  • IF
  • F

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 40-60
    Source/Isotype Rabbit IgG
    Application Key:
    • IHC-Immunohistochemistry 
    • IF-Immunofluorescence 
    • F-Flow Cytometry 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Immunohistochemistry (Paraffin) 1:50 - 1:200
    Immunofluorescence (Immunocytochemistry) 1:400 - 1:1600
    Flow Cytometry (Fixed/Permeabilized) 1:200 - 1:800
    Flow Cytometry (Live) 1:1800 - 1:7200

    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

    DLK1 (F7O3Q) Rabbit mAb recognizes endogenous levels of total DLK1 protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the extracellular domain of human DLK1 protein.

    Background

    Delta-like-1 homolog (DLK1), also known as fetal antigen 1 (FA1) and preadipocyte factor 1 (pref-1), is a member of the epidermal growth factor (EGF)-like family of proteins, containing six tandem EGF-like repeats (1,2). DLK1 is a paternally expressed, imprinted gene that plays an important role in normal development and in the maintenance of homeostasis of adipose tissue mass (3). DLK1-deficient mice display growth retardation, obesity, skeletal malformation, and increased serum lipid metabolites (4). It has been reported that the ectodomain of DLK1 is shredded from the cell surface and inhibits adipocyte differentiation (5-7).

    Humans and rodents express multiple isoforms of DLK1, which are either membrane bound or contain an ADAM17/TACE cleavage site for release of the soluble ectodomain (8). As high DLK1 expression is pro-oncongenic in some contexts, differential isoform expression may promote cancer cell survival, with both the ectodomain and intracellular domain having distinct functions (9). Under hypoxic conditions, HIF proteins induce ADAM17/TACE cleavage and internalization of the DLK1 intracellular domain, which localizes to the nucleus and alters Akt and p53 signaling cascades in glioma (10). Hypoxia increases DLK1 expression, and phosphorylation of the DLK1 C-terminus at Tyr339 and Ser355 increases neuronal tumor sphere growth (11). Nuclear DLK1 directly interacts with tumor supressor NCoR1, correlating with poor prognosis in non small cell lung cancer (NSCLC) (12). DLK1 has emereged as a target for novel antibody drug conjugates (ADCs) in neuroblastoma and adrenocortical carcinoma (13,14).
    For Research Use Only. Not For Use In Diagnostic Procedures.
    Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.
    All other trademarks are the property of their respective owners. Visit our Trademark Information page.