|Cat. No. 218 211BT||100 µg purified IgG, lyophilized, biotin-labeled. For reconstitution add 100 µl H2O to get a 1mg/ml solution in PBS. Then aliquot and store at -20°C until use.|
WB: 1 : 500 up to 1 : 1000 (see remarks)
IP: not tested yet
ICC: not tested yet
IHC: 1 : 100 up to 1 : 500 (see remarks) gallery
IHC-P/FFPE: 1 : 200 up to 1 : 500 gallery
ELISA: yes (see remarks)
|Subtype||IgG2b (κ light chain)|
|Immunogen||Synthetic peptide corresponding to AA 1 to 16 from human Abeta (UniProt Id: P05067)|
Epitop: AA 4 to 8 from human Abeta (UniProt Id: P05067)
Reacts with: human (P05067), mouse (P12023).
Other species not tested yet.
|Specificity||Specific for Abeta 38, 40, 42, 43.|
WB: Boil membrane after blotting for 3min.
IHC: Antigen retrieval with formic acid is required.
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.