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Abeta-pE11 - 218 603

A major component of neuritic plaques in Alzheimer's disease
Polyclonal rabbit purified antibody
Cat. No.: 218 603
Amount: 50 µg
Price: $370.00
Cat. No. 218 603 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 (see remarks) gallery  
IHC-P/FFPE: 1 : 100 (see remarks) gallery  
ELISA: yes (see remarks) gallery  
Immunogen Synthetic peptide corresponding to AA 11 to 16 from human Abeta-pE11 (UniProt Id: P05067)
Reactivity Reacts with: human (P05067), rat (P08592), mouse (P12023).
Other species not tested yet.
Specificity Specific for Abeta-pE11.
Remarks

WB: Detects purified Abeta-pE11. complex samples like brain extracts not tested yet. 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 detector antibody.

Data sheet 218_603.pdf

References for Abeta-pE11 - 218 603

The Arctic AβPP mutation leads to Alzheimer's disease pathology with highly variable topographic deposition of differentially truncated Aβ.
Kalimo H, Lalowski M, Bogdanovic N, Philipson O, Bird TD, Nochlin D, Schellenberg GD, Brundin R, Olofsson T, Soliymani R, Baumann M, et al.
Acta neuropathologica communications (2013) 1: 60. 218 603 IHC; tested species: human
Cat. No.: 218 603
Quantity: 50 µg
Price: $370.00
The Arctic AβPP mutation leads to Alzheimer's disease pathology with highly variable topographic deposition of differentially truncated Aβ.
Kalimo H, Lalowski M, Bogdanovic N, Philipson O, Bird TD, Nochlin D, Schellenberg GD, Brundin R, Olofsson T, Soliymani R, Baumann M, et al.
Acta neuropathologica communications (2013) 1: 60. 218 603 IHC; tested species: human
Background

Amyloid deposits, also called plaques, of Alzheimer's patients consist of several protein components like the amyloid beta-peptides (Abeta, ) 1-40/42 and additional C- and N-terminally truncated and modified fragments. Very abundant are the isoaspartate (isoAsp)-Abeta and pyroglutamyl (pGlu)-Abeta peptides. The latter are formed by cyclization of the N-terminal glutamate at position 3 or 11 catalyzed by glutaminyl cyclase (QC) resulting in very amyloidogenic and neurotxic variants of Abeta; Abeta pE3 and Abeta-pE11.
In contrast to extracellular plaques that do not perfectly correlate with Alzheimer´s disease intraneuronal Abeta accumulation and vascular Abeta deposits have gained more and more evidence to be among the crucial factors responsible for progressive neuron loss.