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Abeta 40 - 218 203

A major component of neuritic plaques in Alzheimer's disease
Polyclonal rabbit purified antibody
Cat. No.: 218 203
Amount: 50 µg
Price: $450.00
Cat. No. 218 203 50 µg specific antibody, lyophilized. Affinity purified with the immunogen. Albumin was 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.
Applications WB: 1 : 1000 (see remarks) gallery  
IP: not tested yet
ICC: not tested yet
IHC: 1 : 200 up to 1 : 500 (see remarks) gallery  
IHC-P/FFPE: 1 : 100 up to 1 : 500 (see remarks) gallery  
ELISA: yes (see remarks) gallery  
Immunogen Synthetic peptide corresponding to AA 33 to 40 from human Abeta40 (UniProt Id: P05067)
Reactivity Reacts with: human (P05067), rat (P08592), mouse (P12023).
Other species not tested yet.
Specificity Specific for Abeta 40, no cross reactivity to Abeta 38 and 42.
Remarks

WB: Detects purified Abeta 40. Complex samples like brain extracts still have to be tested. Boil membrane after blotting for 3min.
IHC: Antigen retrieval with formic acid is required.
IHC-P: Antigen retrieval with formic acid is required.
ELISA: suitable as capture and detector antibody for sandwich-ELISA.

Data sheet 218_203.pdf

References for Abeta 40 - 218 203

Axonal degeneration in an Alzheimer mouse model is PS1 gene dose dependent and linked to intraneuronal Aβ accumulation.
Christensen DZ, Huettenrauch M, Mitkovski M, Pradier L, Wirths O
Frontiers in aging neuroscience (2014) 6: 139. 218 203 IHC
Cat. No.: 218 203
Quantity: 50 µg
Price: $450.00
Axonal degeneration in an Alzheimer mouse model is PS1 gene dose dependent and linked to intraneuronal Aβ accumulation.
Christensen DZ, Huettenrauch M, Mitkovski M, Pradier L, Wirths O
Frontiers in aging neuroscience (2014) 6: 139. 218 203 IHC
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.