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Abeta38/40/42/43 antibody - 218 111BT

Abeta peptides are major components of neuritic plaques in Alzheimer's disease
Mouse monoclonal purified IgG
Cat. No.: 218 111BT
Amount: 100 µg
Price: $465.00
Cat. No. 218 111BT 100 µg purified IgG, lyophilized, labeled with Biotin.

Biotin is a small vitamin B complex molecule. Its small size minimizes interference with antibody binding sites and allows for efficient conjugation without compromising antibody functionality.
Biotin conjugated antibodies can be easily detected with Avidin/Streptavidin based secondary detection systems.
The streptavidin-biotin bond is one of the strongest non-covalent biological bonds known.

For reconstitution add 100 µl H2O to get a 1mg/ml solution in PBS. Then aliquot and store at -20°C to -80°C until use.
Antibodies should be stored at +4°C when still lyophilized. Do not freeze!
Applications
 
WB: 1 : 500 up to 1 : 1000 (see remarks)
IP: not tested yet
ICC: not tested yet
IHC: 1 : 200 up to 1 : 500 (see remarks) gallery  
IHC-P: 1 : 200 up to 1 : 500 (see remarks) gallery  
Label biotin
Clone NT78
Subtype IgG2b (κ light chain)
Immunogen Synthetic peptide corresponding to AA 1 to 16 from human Abeta (UniProt Id: P05067)
Epitop Epitop: AA 4 to 16 from human Abeta (UniProt Id: P05067)
Reactivity Reacts with: human (P05067), mouse (P12023).
Other species not tested yet.
Specificity Specific for Abeta 38, 40, 42, 43.
Remarks

WB: Boil membrane after blotting for 3min.
IHC: Antigen retrieval with formic acid is required.
IHC-P: Antigen retrieval with formic acid is required.

Data sheet 218_111bt.pdf
Cat. No.: 218 111BT
Amount: 100 µg
Price: $465.00
Background

Amyloid deposits, also called plaques, of Alzheimer's patients consist of several protein components like the amyloid beta-peptides (Abeta, Aβ) 1-40/42/43 and additional C- and N-terminally modified fragments of Abeta as for instance Abeta pE3 and Abeta pE11.
An additional Abeta variant, Abeta 38, is more soluble compared to other Abeta species and is not found in plaques of sporadic Alzheimer´s cases. However, it is detected in the blood-vessel walls of a subset of patients with severe cerebral amyloid angiopathy. It especially accumulates in brains of patients carrying mutations in the Abeta coding region.
Cleavage of amyloid precursor protein APP by β- and γ- secretases results in the generation of the Aβ (βA4)peptide, whereas α-secretase cleaves within the Aβ sequence and prevents the formation of Abeta from APP.