Anti-Beta-Amyloid 1-42 Antibody (6J263) is a Mouse antibody targeting Beta-Amyloid 1-42. Anti-Beta-Amyloid 1-42 Antibody (6J263) can be used in IF,IHC-Fr,IHC-P,WB.

IgG2b

6J263

Human (predicted:Mouse,Rat)

1. Positive sample (left): Alzheimer/s Disease Brain
Negative sample (right): Normal Human Brain
Block endogenous peroxidase by 3% hydrogen peroxide for 20 min; Blocking buffer (normal goat serum) at 37°C for 30 min; Incubation with (beta-Amyloid (1-42)) Monoclona Antibody, Unconjugated (TMAB-00226) at 1:1000 overnight at 4°C, followed by operating according to SP Kit (Rabbit) instructionsand DAB staining.
2. 100 ng Aβ1-42 Peptide per Lane probed with beta-Amyloid (1-42) polyclonal antibody respectively, unconjugated (TMAB-00226) at 1:1000 dilution and 4°C overnight incubation. Followed by corresponding conjugated secondary antibody incubation at RT for 60 min.

WB: 1:500-2000; IHC-P: 1:500-5000; IHC-Fr: 1:500-5000; IF: 1:200-5000

Monoclonal

KLH conjugated synthetic peptide: human beta-Amyloid(1-42)

Human

APP

Amyloid-beta precursor protein

Regulation,RNA Processing,DNA / RNA binding

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. 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. Promotes both tau aggregation and TPK II-mediated phosphorylation. Interaction with overexpressed HADH2 leads to oxidative stress and neurotoxicity. Appicans elicit adhesion of neural cells to the extracellular matrix and may regulate neurite outgrowth in the brain. 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).