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Abeta38/40/42/43 antibody - 218 008

Abeta peptides are major components of neuritic plaques in Alzheimer's disease
Rabbit monoclonal recombinant IgG
Cat. No.: 218 008
Amount: 50 µg
Price: $415.00
Cat. No. 218 008 50 µg purified recombinant IgG, lyophilized. Albumin and azide were added for stabilization. For reconstitution add 50 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: not tested yet
IP: not tested yet
ICC: not tested yet
IHC: 1 : 500 up to 1 : 1000 (see remarks) gallery  
IHC-P: 1 : 4000 gallery  
Clone RbNT244
Subtype IgG1 (κ light chain)
Immunogen Synthetic peptide corresponding to AA 1 to 16 from human Abeta (UniProt Id: P05067)
Epitop Epitop: AA 4 to 8 from human Abeta (UniProt Id: P05067)
Reactivity Reacts with: mouse (P12023), human (P05067).
Other species not tested yet.
Specificity Specific for Abeta 38, 40, 42, 43. Due to sequence homology, a cross-reactivity to unprocessed APP cannot be excluded.
Remarks

This antibody is a chimeric antibody based on the monoclonal mouse antibody NT244. The constant regions of the heavy and light chains have been replaced with rabbit specific sequences. The antibody can therefore be used with standard anti-rabbit secondary reagents. The antibody has been expressed in mammalian cells.
IHC: Antigen retrieval with formic acid is required.

Data sheet 218_008.pdf
Cat. No.: 218 008
Amount: 50 µg
Price: $415.00
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, Abeta38, 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.