Catalogue Number: BS-0104M-BSS
| Manufacturer: | Bioss Inc |
| Shelf Life: | 12 months |
| Type: | Polyclonal Primary Antibody - Unconjugated |
| Alias: | 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 |
| Shipping Condition: | Blue Ice |
| Unit(s): | 100 ul |
| Host name: | Mouse |
| Clone: | |
| Isotype: | IgG |
| Immunogen: | KLH conjugated synthetic peptide of human beta-Amyloid(1-16) |
| Application: | IF, IHC-P, WB, IHC-Fr |
Description: 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.
APP
351
P05067
Protein A purified
1 ug/ul
Polyclonal
Unmodified
Store at -20°C for 12 months.