|Amyloid Beta-Peptide (12-28) (human) Catalog No.GP10049|
Sample solution is provided at 25 µL, 10mM.
PC12 pheochromocytoma cell lines are routinely cultured in Dulbecco's modified Eagle's medium containing 10% fetal bovine serum,5% horse serum, 1% glutamine and 1% penicillin/streptomycin. Exponentially growing cellsare plated at 30000 cells per well per 100 µL of fresh medium in 96-well tissue cultures plates. Toxicity assays are carried out by measurementof MTT reduction. Two days after plating PC12 pheochromocytoma cell lines are treated with different concentrations of aged β-amyloid (12-28). After 22 h, MTT (5 mg/mL) wasadded and incubation is continued for a further2 h. Cells are lysed and after 24 h at 37°C,colorimetric determination of MTT reduction is made at 550 nm. Positive controls consist of cells in culture medium. Assay values obtained with these controls are taken as 100% viability.
. Rabanal F, et al. Structural, kinetic and cytotoxicity aspects of 12-28 beta-amyloid protein fragment: a reappraisal. J Pept Sci. 2002 Oct;8(10):578-88.
|Solubility||≥195.5mg/mL in DMSO||Storage||Desiccate at -20°C|
|General tips||For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.|
|Shipping Condition||Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
Amyloid beta (Aǂ or Abeta) is a peptide of 36-43 amino acids that is processed from the Amyloid precursor protein. While best known as a component of amyloid plaques in association with Alzheimer's disease, evidence has been found that Aǂ is a highly multifunctional peptide with significant non-pathological activity1. Aǂ is the main component of deposits found in the brains of patients with Alzheimer's disease. Brain Aǂ is elevated in patients with sporadic Alzheimeros disease. Aǂ is the main constituent of brain parenchymal and vascular amyloid, it contributes to cerebrovascular lesions and is neurotoxic2.
1. Lahiri DK, Maloney B (September 2010). "Beyond the signaling effect role of amyloid-ǂ42 on the processing of AǂPP, and its clinical implications". Exp. Neurol. 225 (1): 51-4.
2. Hardy J, Duff K, Hardy KG, Perez-Tur J, Hutton M (September 1998). "Genetic dissection of Alzheimer's disease and related dementias: amyloid and its relationship to tau". Nat. Neurosci. 1 (5): 355-8.