|Datasheet||Specific References||Reviews||Related Products||Protocols|
|Recombinant Human BACE1 / ASP2 protein (Catalog#10064-HCCH)|
|10 μl/Test, 0.1 mg/ml|
|Aqueous solution containing 0.5% BSA and 0.09% sodium azide|
|This antibody was obtained from a rabbit immunized with purified, recombinant Human BACE1 / ASP2 (rh BACE1 / ASP2; Catalog#10064-HCCH; NP_036236.1; Met 1-Thr 457) and conjugated with FITC under optimum conditions, the unreacted FITC was removed.|
|Human BACE1 / ASP2|
Has cross-reactivity in ELISA with
|This antibody is stable for 12 months from date of receipt when stored at 2℃-8℃. Protected from prolonged exposure to light. Do not freeze !|
Sodium azide is toxic to cells and should be disposed of properly. Flush with large volumes of water during disposal.
Flow cytometric analysis of Human BACE1 expression in Jurkat cells. The cells were treated according to manufacturer’s manual (BD Pharmingen™ Cat. No. 554714), and then stained with FITC Rabbit anti-BACE1 (10064-R027-F). The fluorescence histograms were derived from gated events with the forward and side light-scatter characteristics of intact cells.
Beta-site APP-cleaving enzyme 1 (BACE1) is an aspartic-acid protease important in the formation of myelin sheaths in peripheral nerve cells. In the brain, This protein is expressed highly in the substantia nigra, locus coruleus and medulla oblongata. Strong BACE1 expression has also been described in pancreatic tissue. BACE1 has a pivotal role in the pathogenesis of Alzheimer's disease. In Alzheimer's disease patients, BACE1 levels were elevated although mRNA levels were not changed. It has been found that BACE1 gene expression is controlled by a TATA-less promoter. The translational repression as a new mechanism controlling its expression. And the low concentrations of Ca(2+) (microM range) significantly increased the proteolytic activity of BACE1. Furthermore, BACE1 protein is ubiquitinated, and the degradation of BACE1 proteins and amyloid precursor protein processing are regulated by the ubiquitin-proteasome pathway. It has also been identified as the rate limiting enzyme for amyloid-beta-peptide (Abeta) production.