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beta Amyloid 1-16 (AA 1-16) anticorps

L’anticorps Souris Polyclonal anti- a été validé pour WB, IF (p) et IHC (p). Il convient pour détecter dans des échantillons de Humain.
N° du produit ABIN724955

Aperçu rapide pour beta Amyloid 1-16 (AA 1-16) anticorps (ABIN724955)

Antigène

beta Amyloid 1-16

Reactivité

  • 2
  • 2
Humain

Hôte

  • 2
Souris

Clonalité

  • 2
Polyclonal

Conjugué

  • 2
Inconjugué

Application

  • 2
  • 2
  • 2
  • 2
  • 2
Western Blotting (WB), Immunofluorescence (Paraffin-embedded Sections) (IF (p)), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p))
  • Épitope

    AA 1-16

     Réactivité croisée

    Humain

    Purification

    Purified by Protein A.

    Immunogène

    KLH conjugated synthetic peptide of human beta-Amyloid(1-16)

    Isotype

    IgG
  • Indications d'application

    WB 1:100-1000
    IHC-P 1:100-500
    IF(IHC-P) 1:50-200

    Restrictions

    For Research Use only
  • Format

    Liquid

    Concentration

    1 μg/μL

    Buffer

    Aqueous buffered solution containing 1 % BSA, 50 % glycerol and 0.09 % sodium azide.

    Agent conservateur

    Sodium azide

    Précaution d'utilisation

    This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE, which should be handled by trained staff only.

    Stock

    -20 °C

    Stockage commentaire

    Store at -20°C for 12 months.

    Date de péremption

    12 months
  • Antigène

    beta Amyloid 1-16

    Sujet

    Synonyms: AAA, AD1, PN2, ABPP, APPI, CVAP, ABETA, PN-II, CTFgamma, Amyloid beta A4 protein, APP, Alzheimer disease amyloid protein, Cerebral vascular amyloid peptide, PreA4, Protease nexin-II, A4

    Background: 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.

    ID gène

    351

    UniProt

    P05067
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