MOAB-2: Unprecedented features, unparalleled staining & clarity!
(Image: MOAB-2 does not detect APP in cell culture media, lysates and cortical brain extracts from 5xFAD mice. (A) Western-blot analysis of 5 μg or 15 μg cell lysates from HEK-APPSwe/BACE1 cells, probed with antibodies against C-terminus of APP (CT1565), N-terminus of APP (2211), Aβ (6E10, MOAB-2) or β-Actin (loading control). Notice all the other clones detect APP or APP-CTFs, but that MOAB-2 does not. (B) Western analysis of 25 μg total protein from detergent-extracted 5xFAD mouse cortex probed with 6E10 or MOAB-2 and β-Actin for loading control, demonstrating that MOAB-2 does not detect APP forms, unlike 6E10).
MOAB-2 does not cross react with APP or APP C-terminal fragments
Unlike other monoclonals such as 6E10 and 4G8, MOAB-2 does not cross react with APP or APP C-terminal fragments, which allows isolation and localization of Aß protein from APP.
MOAB-2 preferentially detects pathogenic Aβ42 over Aβ40
In dot blots, MOAB-2 recognizes all forms (unaggregated, oligometric, and fibrillar) of Aβ 42 protein and the unaggregated form of AB40. MOAB-2 is selective for the more neurotoxic Aβ42 compared to Aβ40. In titration tests, MOAB-2 demonstrated a 25 fold greater sensitivity of detection for the U-, O- and F-Aβ42 forms than for Aβ40, demonstrating it is a superb reagent for focusing in on the localization and function of Aβ42.
MOAB-2 is a superb immunohistochemical reagent for the localizing Aβ protein in vivo
Youmans et al. Molecular Neurodegeneration 2012, 7:8
(Image: Coronal sections of the frontal cortex from 1 and 3 month old 5xFAD mice immunostained with 6E10 and MOAB-2 and visualized via DAB staining. Notice how 6E10 is strongly immunoreactive across the field of the cortex, and at higher magnification shows that the cytoplasm is evenly stained with an immunonegative nuclei (A) indicating the detection of both APP and Aβ. In contrast, (B), MOAB-2 staining of sister sections is substantially less than for 6E10 and the intraneuronal staining is punctate. These results are consistent with MOAB-2 recognizing only Aβ and not APP. MOAB-2 reacts in IHC, IH(P) & IF, in all fixations from fresh frozen to archival paraffin embedded tissues.
MOAB-2:Discover intraneuronal Aβ like never before possible, true clarity of staining
(Image: MOAB-2 staining of senile plaque in human Alzheimer's diseased hippocampus formalin fixed paraffin embedded tissues with heat-induced antigen retrieval. Note the depth of clarity and lack of neuronal involvement).
MOAB-2 discriminates between APP and true intraneuronal Aβ in all its forms!
(Image: MOAB-2 detection of intraneuronal Aβ and extracellular plaques in 5xFAD mouse brain tissues. Immunofluorescent detection of Aβ with MOAB-2 in the subiculum of (A) 1, 2 and 4 month old 5xFAD mice. Aβ accumulates extracellularly as the disease progresses making MOAB-2 the ideal reagent for studying both intraneuronal Aβ at early stages and extracellular Aβ at late stages seamlessly).
Biosensis is pleased to bring this new and exciting reagent to the market and we encourage all that have an interest in beta-amyloid or its pathology to try it.
