BACE1产品信息
英文名称:Beta-secretase 1
中文名称:β-分泌酶-1
靶点别称:BACE1,ASP2,BACE,FLJ90568,HSPC104,KIAA1149,Memapsin-2,Beta-Secretase,β-secretase
物种:Human
属性:Protein
标记:Unconjugated
内毒素(Endotoxin)
Less than 1.0 EU per μg by the LAL method.
纯度(Purity)
>98% as determined by SDS-PAGE.
>90% as determined by SEC-MALS.
制剂(Formulation)
Lyophilized from 0.22 μm filtered solution in 50 mM Tris, pH8.0 with trehalose as protectant.
Contact us for customized product form or formulation.
重构方法(Reconstitution)
Please see Certificate of Analysis for specific instructions.
For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.
存储(Storage)
For long term storage, the product should be stored at lyophilized state at -20°C or lower.
Please avoid repeated freeze-thaw cycles.
This product is stable after storage at:
-20°C to -70°C for 12 months in lyophilized state;
-70°C for 3 months under sterile conditions after reconstitution.
BACE1分子背景
Beta-secretase 1 (BACE1) is also known as beta-site APP cleaving enzyme 1 (beta-site amyloid precursor protein cleaving enzyme 1), memapsin-2 (membrane-associated aspartic protease 2), and aspartyl protease 2 (ASP2), β-Secretase , and is a member of the peptidase A1 protein family, BACE1 is a type I integral membrane glycoprotein and aspartic protease that is found mainly in the Golgi. BACE1 is an aspartic-acid protease important in the pathogenesis of Alzheimers disease, and in the formation of myelin sheaths in peripheral nerve cells. The transmembrane protein contains two active site aspartate residues in its extracellular protein domain and may function as a dimer. This protease is responsible for the proteolytic processing of the amyloid precursor protein (APP). Generation of the 40 or 42 amino acid-long amyloid-β peptides that aggregate in the brain of Alzheimers patients requires two sequential cleavages of the APP. Extracellular cleavage of APP by BACE creates a soluble extracellular fragment and a cell membrane-bound fragment referred to as C99. The elevation of BACE1 levels can be induced by amyloid plaques surrounding neurons at early stages of pathology before neuron death occurs, and may drive a positive-feedback loop in AD.