Amyloid Antikörper (Atto 390)

Produktnummer ABIN2486097

Dieses Kaninchen Polyklonal-Antikörper erkennt spezifisch in ELISA, IP, IHC, WB, ICC, IF und DB. Er zeigt eine Reaktivität gegenüber Human.

Kurzübersicht für Amyloid Antikörper (Atto 390) (ABIN2486097)

Target: Amyloid

Reaktivität: Human

Wirt: Kaninchen

Klonalität: Polyklonal

Konjugat: Atto 390

Applikation: ELISA, Immunoprecipitation (IP), Immunohistochemistry (IHC), Western Blotting (WB), Immunocytochemistry (ICC), Immunofluorescence (IF), Dot Blot (DB)

Produktdetails

Spezifität: Recognizes generic epitopes common to many amyloid fibrils and fibrillar oligomers, but not prefibrillar oligomers or natively folded proteins. Expected to detect in Mouse and Rat based on homology.

Kreuzreaktivität: Human

Aufreinigung: Protein A Purified

Immunogen: Fibrils prepared from human amyloid beta 42 peptide

Anwendungsinformationen

Applikationshinweise:

• WB (1:1000)
• IHC (1:100)
• optimal dilutions for assays should be determined by the user.

Kommentare:

A 1:1000 dilution of ABIN2486097 was sufficient for detection of amyloid fibrils on PVDF membranes using transferred fibrils by colorimetric dot blot analysis using Goat anti-rabbit IgG:HRP as the secondary antibody.

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Format: Liquid

Buffer: PBS, 50 % glycerol, 0.09 % sodium azide, Storage buffer may change when conjugated

Konservierungsmittel: Sodium azide

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

Lagerung: 4 °C

Informationen zur Lagerung: Conjugated antibodies should be stored at 4°C

Antigendetails

Target: Amyloid

Hintergrund: Amyloid monomeric proteins can sometimes oligomerize into destructive amyloid fibrils. Amyloidogenic conformations of non-disease related proteins can be created by partial protein misfolding or denaturation. Many degenerative diseases are known to be related to the accumulation of misfolded proteins as amyloid fibres (1, 2). These include the amyloid-β peptide plaques and tau neurofibrillary tangles in senile plaques of Alzheimer's symptomology, the deposition of α-synuclein in the Lewy bodies of Parkinson's disease, and accumulation of polyglutamine-containing aggregates in Huntington's disease (2, 3).