Abcam, ab126649, Anti-beta Amyloid antibody [MOAB-2]

Size: 100µg
Anti-beta Amyloid antibody [MOAB-2] (ab126649) is a mouse monoclonal antibody detecting beta Amyloid in Western Blot, IHC-P . Suitable for Human . - Over 30 publications
Key facts
Host species:Mouse,
Clonality:Monoclonal,
Clone number:MOAB-2,
Isotype:IgG2b,
Carrier free:No,
Reacts with:Human,
Applications:WB, IHC-PSee 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:
Anti-beta Amyloid antibody [MOAB-2] (ab126649) is a mouse monoclonal antibody and is validated for use in IHC-P, WB in human samples.
Anti-beta Amyloid antibody [MOAB-2] (ab126649) has been cited over 30 times in peer reviewed journals and is trusted by the scientific community.
Abcam's high quality validation processes ensure Anti-beta Amyloid antibody [MOAB-2] (ab126649) has high sensitivity and specificity.
Anti-beta Amyloid antibody [MOAB-2] (ab126649) specifically detects beta Amyloid (UniProt ID: P05067; Molecular weight: 85kDa) and is sold in 100 µg selling sizes.
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

Properties and Storage Information:
Form-Liquid, Purification technique-Affinity purification, Storage buffer-pH: 7.4Preservative: 0.02% Sodium azideConstituents: PBS, 6.97% L-Arginine, Shipped at conditions-Blue Ice, Appropriate short-term storage conditions-+4°C, Appropriate long-term storage conditions--20°C, Aliquoting information-Upon delivery aliquot, Storage information-Avoid freeze / thaw cycle

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.