Overview |
bs-0104M |
beta Amyloid 1-16 Polyclonal Antibody |
WB, IHC-P, IF(IHC-P) |
Human |
Specifications |
Unconjugated |
Mouse |
KLH conjugated synthetic peptide of human beta-Amyloid(1-16) |
670-700/770 |
Polyclonal |
IgG |
1ug/ul |
Purified by Protein A. |
Aqueous buffered solution containing 1% BSA, 50% glycerol and 0.09% sodium azide. |
Store at -20°C for 12 months. |
Target |
351 |
P05067 |
Extracellular |
AAA; AD1; PN2; ABPP; APPI; CVAP; ABETA; PN-II; CTFgamma; Amyloid beta A4 protein; APP; Alzheimer disease amyloid protein; Cerebral vascular amyloid peptide; PreA4; Protease nexin-II; A4 |
Functions as a cell surface receptor and performs physiological functions on the surface of neurons relevant to neurite growth, neuronal adhesion and axonogenesis. Involved in cell mobility and transcription regulation through protein-protein interactions. Can promote transcription activation through binding to APBB1-KAT5 and inhibits Notch signaling through interaction with Numb. Couples to apoptosis-inducing pathways such as those mediated by G(O) and JIP. Inhibits G(o) alpha ATPase activity (By similarity). Acts as a kinesin I membrane receptor, mediating the axonal transport of beta-secretase and presenilin 1. Involved in copper homeostasis/oxidative stress through copper ion reduction. In vitro, copper-metallated APP induces neuronal death directly or is potentiated through Cu(2+)-mediated low-density lipoprotein oxidation. Can regulate neurite outgrowth through binding to components of the extracellular matrix such as heparin and collagen I and IV. The splice isoforms that contain the BPTI domain possess protease inhibitor activity. Induces a AGER-dependent pathway that involves activation of p38 MAPK, resulting in internalization of amyloid-beta peptide and leading to mitochondrial dysfunction in cultured cortical neurons. Provides Cu(2+) ions for GPC1 which are required for release of nitric oxide (NO) and subsequent degradation of the heparan sulfate chains on GPC1. Beta-amyloid peptides are lipophilic metal chelators with metal-reducing activity. Bind transient metals such as copper, zinc and iron. In vitro, can reduce Cu(2+) and Fe(3+) to Cu(+) and Fe(2+), respectively. Beta-amyloid 42 is a more effective reductant than beta-amyloid 40. Beta-amyloid peptides bind to lipoproteins and apolipoproteins E and J in the CSF and to HDL particles in plasma, inhibiting metal-catalyzed oxidation of lipoproteins. Beta-APP42 may activate mononuclear phagocytes in the brain and elicit inflammatory responses. |
Application Dilution |
WB |
1:300-5000 |
IHC-P |
1:200-400 |
IF(IHC-P) |
1:50-200 |