Cat. No.: 218 511
Amount: 100 µg
Price:
$420.00
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| Cat. No. 218 511 |
100 µg purified IgG, lyophilized. Albumin and azide were added for stabilization. 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. Antibodies should be stored at +4°C when still lyophilized. Do not freeze! |
| Applications | |
| Important note for users | The mouse monoclonal antibody clone 9D5, Cat. No. 218 511, is patented (patent application PCT/EP2011/002739). By purchasing this antibody the customer acquires rights to use this product for research purposes only. Any diagnostic and therapeutic in vitro or in vivo use is explicitly excluded. |
| Clone | 9D5 |
| Subtype | IgG2b (κ light chain) |
| Immunogen | Synthetic peptide corresponding to AA 3 to 38 from human Oligo-Abeta-pE3 (UniProt Id: P05067) |
| Reactivity |
Reacts with: human (P05067), mouse (P12023). Other species not tested yet. |
| Specificity | Recognizes specific oligomeric structures formed preferentially by Abeta-pE3. |
| Remarks |
WB: We recommend the Invitrogen NativePAGE system in combination with PVDF blotting membranes. Boil membrane in PBS after blotting in PBS for 3min.
This antibody has only been validated with synthetic peptides and not with complex protein samples.
Peptide preparation: Synthetic Abeta peptides were monomerized in 70 % formic acid, and the solvent was evaporated in a speed-vac immediately. Prior to each experiment, peptides were dissolved in 0.3 % ammonia, underwent ultrasonic treatment, and were further diluted to an end concentration of 0.15 % ammonia. |
| Data sheet | 218_511.pdf |
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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.