β-Amyloid 40 (human) (rec.)
Activity has not been tested.
|Formulation||Liquid in 20mM HEPES, pH 7.0, Glycerol.|
|Other Product Data||
Click here for Original Manufacturer Product Datasheet
|Declaration||Manufactured by AbFrontier|
|Shipping and Handling|
|Short Term Storage||-20°C|
|Long Term Storage||-80°C|
|Handling Advice||Avoid freeze/thaw cycles.|
|Product Specification Sheet|
β-amyloid (Aβ) peptides result from the proteolytic cleavage of β-amyloid precursor protein (APP) which is encoded by a gene located on chromosome 21. Aβ is produced by two proteases (β- and γ- secretase) and has vary forms (39- and 43-mer peptides). Aβ40 and Aβ42 peptides are major constituents of the plaques and tangles that occur in Alzheimer’s disease(AD). Aβ42 plays a critical role in the pathogenesis of AD since its aggregative ability and neurotoxicity are much greater than these of Aβ40. Aβ42 oligomers initially formed as a seed accelerate the aggregation of Aβ40 to form the amyloid plaques that eventually lead to the neurodegeneration (amyloid cascade hypothesis). Aβ40 also serves as an antioxidant molecule by quenching metal ions and inhibiting metal-mediated oxygen radical generation.
1) Kazuhiro Irie et al. (2005) Journal of bioscience and bioengineering 99(5):437-447. (General)
2) Andreas Kern et al. (2005) Journal of Biological Chemistry. (General)
3) John hardy et al. (2002) Science 297(19):353-356. 4. Zou K. et al. (2003) J Neurochem. 87(3):609-619. (General)