Detects human and mouse BACE-1 in direct ELISAs and human BACE-1 in Western blots. In Western blots, no cross-reactivity with recombinant human (rh) BACE-2, recombinant mouse (rm) BACE-2, rhADAM8, rmADAM9, rmADAM10, rhADAM15, or rhTACE is observed.
Monoclonal Mouse IgG1 Clone # 137612
Protein A or G purified from hybridoma culture supernatant
Mouse myeloma cell line NS0-derived recombinant human BACE-1 Thr22-Tyr460 Accession # P56817
Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. *Small pack size (SP) is supplied as a 0.2 µm filtered solution in PBS.
Detection of Human BACE‑1 by Western Blot.
Western blot shows lysates of human brain (Alzheimer's disease hippocampus) tissue. PVDF Membrane was probed with 2 µg/mL of Mouse Anti-Human/Mouse BACE‑1 Ectodomain Monoclonal Antibody (Catalog # MAB931) followed by HRP-conjugated Anti-Mouse IgG Secondary Antibody (Catalog # HAF007). Specific bands were detected for BACE‑1 at approximately 60 and 70 kDa (as indicated). This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 1.
Preparation and Storage
Reconstitute at 0.5 mg/mL in sterile PBS.
Reconstitution Buffer Available
The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. *Small pack size (SP) is shipped with polar packs. Upon receipt, store it immediately at -20 to -70 °C
Stability & Storage
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
12 months from date of receipt, -20 to -70 °C as supplied.
1 month, 2 to 8 °C under sterile conditions after reconstitution.
6 months, -20 to -70 °C under sterile conditions after reconstitution.
BACE-1 (beta‑site APP cleaving enzyme-1) is an aspartic protease and an integral membrane protein (1, 2). It is the major beta secretase, and together with the gamma secretase, is responsible for generating the amyloid beta peptide (A beta ) from the amyloid precursor protein (APP) (3, 4). Because A beta is a major component of amyloid plaques, BACE-1 has been implicated in the onset and/or progression of Alzheimer's disease. High levels of BACE-1 activity are sufficient to elicit neurodegeneration and neurological decline in vivo, indicating that inhibiting BACE-1 may block not only A beta -dependent but also A beta -independent pathogenic mechanisms (5). In addition to APP, BACE-1 also cleaves APP-like proteins 1 and 2, the cell adhesion protein P-selectin glycoprotein ligand-1 and beta -galactoside alpha 2,6-sialyltransferase, implying that BACE-1 may have additional functions involving the ectodomain shedding of membrane proteins (6‑8).
Vassar, R. et al. (1999) Science 286:735.
Yan, R. et al. (1999) Nature 402:533.
Cai, H. et al. (2001) Nature Neurosci. 4:233.
Roberds, S.L. et al. (2001) Human Mol. Genet. 97:1317.
Rockenstein, E. et al. (2005) J. Biol. Chem. 280:32957.
Li, Q and T.C. Sudhof (2004) J. Biol. Chem. 279:10542.
Lichtenthaler, S.F. et al. (2003) J. Biol. Chem. 278:48713.
Kitazynem, S. et al. (2005) J. Biol. Chem. 280:8589.
beta-site Ayloid Precursor Protein Cleaving Enzyme 1
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