Render Target: SSR
Render Timestamp: 2024-10-24T19:41:34.257Z
Commit: 56767fe525c928647c8401233a175d0d607d385d
XML generation date: 2024-09-30 01:56:13.912
Product last modified at: 2024-09-30T08:00:43.223Z
1% for the planet logo
PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

Lunatic Fringe (D6V2V) Rabbit mAb #66472

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H M R Mk
    SENSITIVITY Endogenous
    MW (kDa) 42
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Mk-Monkey 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:200

    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

    Lunatic Fringe (D6V2V) Rabbit mAb recognizes endogenous levels of total Lunatic Fringe protein.

    Species Reactivity:

    Human, Mouse, Rat, Monkey

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu74 of human Lunatic Fringe protein.

    Background

    Lunatic Fringe (Beta-1,3-N-acetylglucosaminyltransferase, LFNG) is a single-pass type II Golgi membrane glycosyltransferase that catalyzes the elongation of O-linked fucose residues on EGF-like repeats of Notch signaling molecules. Fucosylation of EGF-like repeats serves to fine-tune Notch ligand-receptor interactions, thereby modulating downstream Notch pathway activity (1). Studies in genetic mouse models have shown that Lunatic Fringe-mediated Notch regulation is critical for somite patterning during vertebrate embryogenesis (2-4). Consistent with this, loss-of-function mutations in human LFNG are associated with spondylocostal dysostoses, a heritable skeletal growth disorder characterized by malformations of the spinal column and thoracic structures (5). Lunatic Fringe continues to modulate Notch signaling postnatally (6), and is implicated as a putative tumor suppressor in multiple Notch-related cancers (7, 8).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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