Amyloid Beta A4 Protein

E1836Mo

Sandwich

48T,96T

5.36ng/mL

10-2000ng/mL

Serum, plasma, cell culture supernates

Mouse

2-8ºC

1h 30m

Functions as a cell surface receptor and performs physiological functions on the surface of neurons relevant to neurite growth, neuronal adhesion and axonogenesis. Interaction between APP molecules on neighboring cells promotes synaptogenesis. Involved in cell mobility and transcription regulation through protein-protein interactions. Can promote transcription activation through binding to APBB1-KAT5 and inhibit 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 (By similarity). By acting as a kinesin I membrane receptor, plays a role in axonal anterograde transport of cargo towards synapes in axons (By similarity). May be involved in copper homeostasis/oxidative stress through copper ion reduction. Can regulate neurite outgrowth through binding to components of the extracellular matrix such as heparin and collagen I and IV (By similarity). 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 (By similarity). 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. Amyloid-beta Peptides are lipophilic metal chelators with metal-reducing activity. Binds transient metals such as copper, zinc and iron. Rat and mouse amyloid-beta Peptides bind only weakly transient metals and have little reducing activity due to substitutions of transient metal chelating residues. Amyloid-beta protein 42 may activate mononuclear phagocytes in the brain and elicit inflammatory responses. Promotes both tau aggregation and TPK II-mediated phosphorylation. Also binds GPC1 in lipid rafts (By similarity). The gamma-CTF Peptides as well as the caspase-cleaved Peptides, including C31, are potent enhancers of neuronal apoptosis. N-APP binds TNFRSF21 triggering caspase activation and degeneration of both neuronal cell bodies (via caspase-3) and axons (via caspase-6).

86,722

11820

Abeta40;Abeta42;ABPP;AG;AID(50;AID(57;AID(59;Alpha-CTF;Alpha-secretase C-terminal fragment;Alzheimer disease amyloid A4 protein homolog;Amyloid intracellular domain 50;Amyloid intracellular domain 57;Amyloid intracellular domain 59;Amyloid precursor protein;Amyloid-beta A4 protein;Amyloid-beta precursor protein;Amyloid-beta protein 40;Amyloid-beta protein 42;Amyloidogenic glycoprotein;APP;APP-C57;APP-C59;APP-C99;Beta-APP40;Beta-APP42;Beta-CTF;Beta-secretase C-terminal fragment;C31;C80;C83;C99;Gamma-CTF(50;Gamma-CTF(57;Gamma-CTF(59;Gamma-secretase C-terminal fragment 50;Gamma-secretase C-terminal fragment 57;Gamma-secretase C-terminal fragment 59;N-APP;P3(42;S-APP-alpha;P3(40;S-APP-beta;Soluble APP-alpha;Soluble APP-beta

APP

Neuroscience

APP