Render Target: STATIC
Render Timestamp: 2024-12-13T10:57:49.348Z
Commit: 611277b6de3cd1bb065350b6ef8d63df412b7185
XML generation date: 2024-09-30 01:54:41.377
Product last modified at: 2024-11-15T18:45:09.253Z
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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.

SUFU (C81H7) Rabbit mAb #2522

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H M Mk
    SENSITIVITY Endogenous
    MW (kDa) 54
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • Mk-Monkey 

    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, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    SUFU (C81H7) Rabbit mAb detects endogenous level of total SUFU protein.

    Species Reactivity:

    Human, Mouse, Monkey

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ala340 of human SUFU.

    Background

    SUFU (Suppressor of Fused) was identified in Drosophila as a suppressor of the Fused (Fu) kinase that is essential for Hedgehog signaling during embryonic pattern formation (1). SUFU suppresses Hedgehog signaling by regulating the localization of the transcription factors Gli and Ci (2,3). In Drosophila, SUFU may also positively regulate Hedgehog signaling depending on SUFU protein levels and Hedgehog signal intensity (4). SUFU may function as a tumor suppressor as inactivation and loss of heterozygosity of SUFU is associated with human rhabdomyosarcomas and medulloblastomas (5,6). Deletion of SUFU in mice results in embryonic lethality, while heterozygotes exhibit developmental defects characteristic of basal cell nevus syndrome. This aberrant developmental pathway is attributed to ligand-independent activation of Hedgehog signaling (7). GSK-3β binds and phosphorylates SUFU in vitro and additional information predicts that GSK-3β may positively regulate Hedgehog signaling through modification of SUFU (8).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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