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    Anti-Amyloid Precursor Protein Rabbit mAb

    Catalog number :AT0441
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    Functions as a cell surface receptor and performs physiological functions on the surface of neurons relevant to neurite growth, neuronal adhesion and axonogenesis. Involved in cell mobility and transcription regulation through protein-protein interactions. Can promote transcription activation through binding to APBB1-KAT5 and inhibits Notch signaling through interaction with Numb. Couples to apoptosis-inducing pathways such as those mediated by G(O) and JIP. Inhibits G(o) alpha ATPase activity (By similarity). Acts as a kinesin I membrane receptor, mediating the axonal transport of beta-secretase and presenilin 1. Involved in copper homeostasis/oxidative stress through copper ion reduction. In vitro, copper-metallated APP induces neuronal death directly or is potentiated through Cu(2+)-mediated low-density lipoprotein oxidation. Can regulate neurite outgrowth through binding to components of the extracellular matrix such as heparin and collagen I and IV. The splice isoforms that contain the BPTI domain possess protease inhibitor activity. Induces a AGER-dependent pathway that involves activation of p38 MAPK, resulting in internalization of amyloid-beta peptide and leading to mitochondrial dysfunction in cultured cortical neurons. Provides Cu(2+) ions for GPC1 which are required for release of nitric oxide (NO) and subsequent degradation of the heparan sulfate chains on GPC1.
    Beta-amyloid peptides are lipophilic metal chelators with metal-reducing activity. Bind transient metals such as copper, zinc and iron. In vitro, can reduce Cu(2+) and Fe(3+) to Cu(+) and Fe(2+), respectively. Beta-amyloid 42 is a more effective reductant than beta-amyloid 40. Beta-amyloid peptides bind to lipoproteins and apolipoproteins E and J in the CSF and to HDL particles in plasma, inhibiting metal-catalyzed oxidation of lipoproteins. Beta-APP42 may activate mononuclear phagocytes in the brain and elicit inflammatory responses. Promotes both tau aggregation and TPK II-mediated phosphorylation. Interaction with Also bind GPC1 in lipid rafts.
    Appicans elicit adhesion of neural cells to the extracellular matrix and may regulate neurite outgrowth in the brain.
    The gamma-CTF peptides as well as the caspase-cleaved peptides, including C31, are potent enhancers of neuronal apoptosis.
    N-APP binds TNFRSF21 triggering caspase activation and degeneration of both neuronal cell bodies (via caspase-3) and axons (via caspase-6).
    Overview
    Description
    Rabbit monoclonal antibody to Amyloid beta precursor protein
    Reactivity
     Mouse, Rat, Human, Macaque Monkey
    Tested applications
    WB: 1/500 - 1/2000. Detects a band of approximately 116 kDa.

    IHC-P: Use at an assay dependent dilution. Requires denatured and reduced sample to allow access to epitope.

    ICC: 1/100 - 1/500. Requires denatured and reduced sample to allow access to epitope.

    IP: Use at an assay dependent dilution.
    Properties
    Immunogen

    Synthetic peptide from within human KPI domain of human APP751/770 conjugated to Keyhole Limpet Heamocyanin (KLH)

    Clonality
    Monoclonal, clone number: 4EW1
    Isotype
    Rabbit IgG
    Form
    Liquid
    Storage instruction
    Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
    Database links
    Applications
    WB Image


    Western blot - Amyloid beta precursor protein antibody

    Soluble extract of macaque brain (Macaca fasicularis, lanes 1, 3, 5) or conditioned medium from CHO cells expressing recombinant human APP770 (lanes 2, 4, 6) were separated by 7.5% SDS-PAGE, transferred to nitrocellulose and immunoblotted with the following antibodies:

    Lanes 1 and 2 = mouse monoclonal antibody to b-amyloid 1-17 of APP


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