Render Target: SSR
Render Timestamp: 2025-03-06T19:09:19.366Z
Commit: 9fc0f116116d9da247dc8ddd4e5fe811153412e1
XML generation date: 2024-08-01 15:23:35.004
Product last modified at: 2025-01-01T09:04:51.456Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

FE65 Antibody #2877

Filter:
  • WB

    Supporting Data

    REACTIVITY M R
    SENSITIVITY Endogenous
    MW (kDa) 100
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • M-Mouse 
    • R-Rat 

    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 and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    FE65 Antibody detects endogenous levels of FE65. It does not cross-react with FE65L1 or FE65L2.

    Species Reactivity:

    Mouse, Rat

    The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.

    Species predicted to react based on 100% sequence homology:

    Human

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues of human FE65. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    FE65, FE65L1, and FE65L2 are members of the FE65 protein family. FE65 is an adaptor protein with protein-protein interaction domains, including a WW domain followed by two phosphotyrosine interaction domains (PID1 and PID2) (1). Amyloid-β (Aβ) precursor protein (APP) binds to PID2 and undergoes sequential cleavage. First, α-/β secretases cleave and release the ectodomain into the extracellular environment. Subsequent processing by the γ-secretase complex results in the APP intracellular domain (AICD) and the Aβ peptides. The latter Aβ fragments form the main components of amyloid plaques in patients with Alzheimer's disease (2). FE65 family members can regulate APP processing, resulting in elevated levels of Aβ (3). Double knockout mice of FE65 and FE65L1 display a phenotype that occurs in animals lacking APP family members, supporting a functional interaction between FE65 and APP (4).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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