Anti-Amyloid β A4 (Phospho-Thr743/668) antibody
Specifications
| Product Cat#: | AB-07-2350 |
| Product type: | Primary antibody |
| Antigen: | Amyloid β A4 |
| Immunogen: | A synthetic peptide derived from human Amyloid β A4 around the phosphorylation site of threonine 743 (A-V-TP-P-E). The exact amino-acid sequence is proprietary. |
| Species immunized: | Rabbit |
| Isotype: | IgG |
| Applications: | Western Blot (1:500-1:2500); ELISA (1:10000); Immunohistochemistry (1:50-1:100); Immunofluorescence (1:100-1:500) |
| Reactivity: | Human, Mouse, Rat |
| Clonality (clone number): | Polyclonal |
| Form: | Liquid |
| Buffer: | PBS (without Mg2+ and Ca2+ ), pH 7.4, 0.02% sodium azide and 50% glycerol |
| Concentration: | 1 mg/ml |
| Purity: | Antigen affinity chromatography |
| Storage: | Aliquot and freeze at -20°C. Avoid multiple freeze/thaw cycles. |
| Alternative names: | A4, ABPP, AD1, APP, APPI, Alzheimer's disease amyloid protein, Amyloid beta A4 protein precursor, Beta-amyloid protein 40, Beta-amyloid protein 42, C31, C83, CVAP, Cerebral vascular amyloid peptide, Gamma-CTF(50), Gamma-CTF(57), Gamma-CTF(59), P3(40), P3(42), PN-II, PreA4, Protease nexin-II, Soluble APP-alpha (S-APP- alpha), Soluble APP-beta (S-APP-beta) |
Target information
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 (PubMed:25122912). 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.
Provider
Erpantech Laboratory
