ELISA APP Antibody, Biotin

Quantity :50µg Clone Number: Aliases:A4 antibody; A4_ antibody; AAA antibody; ABETA antibody; ABPP antibody; AICD-50 antibody; AICD-57 antibody; AICD-59 antibody; AID(50) antibody; AID(57) antibody; AID(59) antibody; Alzheimer disease amyloid protein antibody; Amyloid intracellµLar domain 50 antibody; Amyloid intracellµLar domain 57 antibody; Amyloid intracellµLar domain 59 antibody; APP antibody; APPI antibody; Beta amyloid protein 42 antibody; Beta APP42 antibody; Beta-APP40 antibody; Beta-APP42 antibody; C31 antibody; Cerebral vascµLar amyloid peptide antibody; CVAP antibody; Gamma-CTF(50) antibody; Gamma-CTF(57) antibody; Gamma-CTF(59) antibody; PN-II antibody; PreA4 antibody; Protease nexin-II antibody; S-APP-alpha antibody; S-APP-beta antibody Product Type:Polyclonal Antibody Immunogen Species:Homo sapiens () UniProt ID:P05067 Immunogen:Recombinant Amyloid-beta A4 protein (18-270AA) Raised in:Rabbit Reactivity: Tested Applications:ELISA Background: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 regµLation throµgh protein-protein interactions. Can promote transcription activation throµgh binding to APBB1-KAT5 and inhibits Notch signaling throµgh 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 throµgh copper ion reduction. In vitro, copper-metallated APP induces neuronal death directly or is potentiated throµgh Cu2+-mediated low-density lipoprotein oxidation. Can regµLate neurite outgrowth throµgh binding to components of the extracellµLar 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, resµLting in internalization of amyloid-beta peptide and leading to mitochondrial dysfunction in cµLtured cortical neurons. Provides Cu2+ ions for GPC1 which are required for release of nitric oxide (NO) and subsequent degradation of the heparan sµLfate chains on GPC1. Ref.38 Ref.65 Ref.67 Ref.90 Ref.91 Beta-amyloid peptides are lipophilic metal chelators with metal-reducing activity. Bind transient metals such as copper, zinc and iron. In vitro, can reduce Cu2+ and Fe3+ to Cu+ and Fe2+, 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. Promotes both tau aggregation and TPK II-mediated phosphorylation. Interaction with Also bind GPC1 in lipid rafts. Clonality:Polyclonal Isotype:IgG Purification Method:>95%, Protein G purified Conjµgate:Biotin Buffer:Preservative: 0.03% Proclin 300 Constituents: 50% Glycerol, 0.01M PBS, PH 7.4 Form:Liquid Stroage:Upon receipt, store at -20°C or -80°C. Avoid repeated freeze. Target Names:APP Research Areas:Neuroscience