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

Produktnummer ABIN724955

Produktdetails

Target: beta Amyloid 1-16

Bindungsspezifität: AA 1-16

Reaktivität: Human

Wirt: Maus

Klonalität: Polyklonal

Konjugat: Unkonjugiert

Applikation: Western Blotting (WB), Immunofluorescence (Paraffin-embedded Sections) (IF (p)), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p))

Kreuzreaktivität: Human

Aufreinigung: Purified by Protein A.

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

Isotyp: IgG

Anwendungsinformationen

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

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Format: Liquid

Konzentration: 1 μg/μL

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

Konservierungsmittel: Sodium azide

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

Lagerung: -20 °C

Informationen zur Lagerung: Store at -20°C for 12 months.

Haltbarkeit: 12 months

Antigendetails

Target: beta Amyloid 1-16

Hintergrund:

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.

Gen-ID: 351

UniProt: P05067