Human VEGF121 Protein, His Tag-null-试剂-生物在线
北京百普赛斯生物科技股份有限公司
Human VEGF121 Protein, His Tag

Human VEGF121 Protein, His Tag

商家询价

产品名称: Human VEGF121 Protein, His Tag

英文名称: Human VEGF121 Protein, His Tag

产品编号: VE1-H5246

产品价格: 0

产品产地: USA

品牌商标: ACROBiosystems

更新时间: null

使用范围: null

北京百普赛斯生物科技股份有限公司
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  • 邮箱 : order.cn@acrobiosystems.com

分子量:75 kDa

纯度:>85% as determined by SDS-PAGE.

内毒素:Less than 1.0 EU per μg of the Human BACE-1, Fc Tag by the LAL method.

Buffer:50 mM tris, 100 mM glycine, pH7.5

生物活性:Measured by its ability to cleave a fluorogenic peptide substrate, Mca-SEVNLDAEFRK (Dpn) RR-NH2.  The specific activity is > 1.5 pmoles /min /μg.

产品特性:Human BACE-1, Fc Tag is fused with a human IgG1 Fc tag at the N-terminus, and has a calculated MW of 75 kDa. The predicted N-terminus is Glu. The reducing (R) protein migrates as 100-110 kDa in SDS-PAGE  due to glycosylation.

产品背景: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 Alzheimer's 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 Alzheimer's 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. 
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