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Abeta-pE11 - 218 811

A major component of neuritic plaques in Alzheimer's disease
Monoclonal mouse purified IgG
Cat. No.: 218 811
Amount: 100 µg
Price: $415.00
Cat. No. 218 811 100 µg purified IgG, lyophilized. Azide was added before lyophilization. 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.
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 : 500 (see remarks) gallery  
Clone 173D8
Subtype IgG2b (κ light chain)
Immunogen Synthetic peptide corresponding to AA 11 to 16 from human Abeta-pE11 (UniProt Id: P05067)
Epitop Epitop: 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.

Data sheet 218_811.pdf

References for Abeta-pE11 - 218 811

The presubiculum is preserved from neurodegenerative changes in Alzheimer's disease.
Murray CE, Gami-Patel P, Gkanatsiou E, Brinkmalm G, Portelius E, Wirths O, Heywood W, Blennow K, Ghiso J, Holton JL, Mills K, et al.
Acta neuropathologica communications (2018) 61: 62. 218 811 IHC-P; tested species: human
Cat. No.: 218 811
Quantity: 100 µg
Price: $415.00
The presubiculum is preserved from neurodegenerative changes in Alzheimer's disease.
Murray CE, Gami-Patel P, Gkanatsiou E, Brinkmalm G, Portelius E, Wirths O, Heywood W, Blennow K, Ghiso J, Holton JL, Mills K, et al.
Acta neuropathologica communications (2018) 61: 62. 218 811 IHC-P; 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.