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BRAND / VENDOR: Abcam

Abcam, ab230297, Anti-beta Amyloid antibody [MOAB-2] - BSA and Azide free

CATALOG NUMBER: ab230297
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Product Description

Size: 100µg
Mouse Monoclonal Amyloid-beta precursor protein antibody. Carrier free. Suitable for IHC-P, WB and reacts with Human samples. Cited in 2 publications.
Key facts
Host species:Mouse,
Clonality:Monoclonal,
Clone number:MOAB-2,
Isotype:IgG2b,
Carrier free:Yes,
Reacts with:Human,
Applications:IHC-P, WBSee reactivity dataSee the reactivity data table below for information on validated species and application combinations.,
Immunogen:The exact immunogen used to generate this antibody is proprietary information.

Product details:
ab230297 is the carrier-free version of
ab126649
The clone name for this antibody is also known as 6C3.
Want a custom formulation?
This antibody clone is manufactured by Abcam. If you require a custom buffer formulation or conjugation for your experiments, please contact orders@abcam.com
Conjugation ready
Our carrier-free antibodies are typically supplied in a PBS-only formulation, purified and free of BSA, sodium azide and glycerol. This conjugation-ready format is designed for use with fluorochromes, metal isotopes, oligonucleotides, and enzymes, which makes them ideal for antibody labelling, functional and cell-based assays, flow-based assays (e.g. mass cytometry) and Multiplex Imaging applications.
Use our
conjugation kits
for antibody conjugates that are ready-to-use in as little as 20 minutes with 1 minute hands-on-time and 100% antibody recovery: available for fluorescent dyes, HRP, biotin and gold.
Compatibility
This product is compatible with the Maxpar
Antibody Labeling Kit from Fluidigm, without the need for antibody preparation. Maxpar
is a trademark of Fluidigm Canada Inc.

Properties and Storage Information:
Form-Liquid, Purification technique-Affinity purification, Storage buffer-Constituents: PBS, Shipped at conditions-Blue Ice, Appropriate short-term storage conditions-+4°C, Appropriate long-term storage conditions-+4°C, Storage information-Do Not Freeze

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Beta amyloid also known as amyloid beta peptide is a small protein fragment composed of 36-43 amino acids. It typically has a mass of approximately 4 kDa. This peptide primarily emerges from the amyloid precursor protein (APP) through enzymatic actions by beta-secretase and gamma-secretase. Beta amyloid is commonly expressed in the brain particularly within the neuronal tissue. It is known for aggregating into insoluble fibrils leading to the formation of beta amyloid plaques. Researchers often study beta amyloid using tools like amyloid beta IHC and with specific antibodies like moab 2 and 2e9 which help in detecting its presence and distribution.
Biological function summary
In the context of neuronal function beta amyloid is significant yet contentious. It is believed to play a role in synaptic transmission and may partake in homeostatic regulation. However the true physiological role still remains not well defined. Beta amyloid often self-assembles into oligomers and further into beta amyloid plaques which are part of a larger complex that includes various cellular and molecular components. The plaques contribute to neural pathway disruptions and may interfere with synaptic connections.
Pathways
Beta amyloid integrates into important cellular processes such as the amyloidogenic and non-amyloidogenic pathways. The amyloidogenic pathway involves the sequential cleavage of APP by beta and gamma secretases leading to beta amyloid release which can aggregate. In contrast the non-amyloidogenic pathway mediated by alpha-secretase precludes beta amyloid formation. Proteins such as presenilin-1 and nicastrin are closely tied to beta amyloid formation due to their roles in the gamma-secretase complex.
Beta amyloid is primarily associated with Alzheimer's disease where its accumulations form characteristic amyloid plaques observed in patients' brains. These plaques are implicated in neuronal damage and cognitive decline. Beyond Alzheimer's beta amyloid may also connect to cerebral amyloid angiopathy a condition marked by amyloid deposits in the blood vessels of the brain leading to increased risk of hemorrhagic stroke. Recent studies suggest other proteins such as tau link closely with beta amyloid pathology in Alzheimer's promoting neurofibrillary tangles and synaptic degeneration.


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Collaboration

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