|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.|
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
|Subtype||IgG2b (κ light chain)|
|Immunogen||Synthetic peptide corresponding to AA 11 to 16 from human Abeta-pE11 (UniProt Id: P05067)|
Epitop: AA 11 to 16 from human Abeta-pE11 (UniProt Id: P05067)
Reacts with: human (P05067), rat (P08592), mouse (P12023).
Other species not tested yet.
|Specificity||Specific for Abeta-pE11.|
WB: Detects purified Abeta-pE11. complex samples like brain extracts not tested yet. Boil membrane after blotting for 3min.
Amyloid deposits, also called plaques, of Alzheimer's patients consist of several protein components like the amyloid beta-peptides (Abeta, Aβ) 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.