beta-Amyloid(1-42) Antibody (YA6439)

beta-Amyloid(1-42) Antibody (YA6439) is a mouse-derived and non-conjugated IgG2b monoclonal antibody, targeting to beta-Amyloid (1-42). It can be applicated for WB, IHC-P, IHC-F, IF-Tissue assays, in the background of human.

APP functions as a cell surface receptor on neurons, playing roles in neurite growth, neuronal adhesion, and axonogenesis. Interactions between APP molecules on adjacent cells promote synaptogenesis. It participates in cell mobility and transcription regulation via protein-protein interactions, activating transcription through binding to APBB1-KAT5 while inhibiting Notch signaling via interaction with Numb. It couples to apoptosis pathways (e.g., G(o)- and JIP-mediated) and inhibits G(o) alpha ATPase activity (by similarity). As a kinesin I membrane receptor, it mediates axonal transport of beta-secretase and presenilin 1 (by similarity) and facilitates anterograde cargo transport toward synapses. It contributes to copper homeostasis/oxidative stress by reducing copper ions; copper-metallated APP induces neuronal death directly or via Cu²⁺-mediated LDL oxidation in vitro. By binding extracellular matrix components (e.g., heparin, collagen I/IV), it regulates neurite outgrowth. Splice isoforms containing the BPTI domain exhibit protease inhibitor activity. APP triggers an AGER-dependent pathway involving p38 MAPK activation, leading to amyloid-beta peptide internalization and mitochondrial dysfunction in cortical neurons. It supplies Cu²⁺ ions to GPC1 for NO release and heparan sulfate degradation. Amyloid-beta peptides act as lipophilic metal chelators, reducing Cu²⁺/Fe(3+) to Cu(+)/Fe²⁺ and binding lipoproteins (e.g., apoE/J, HDL) to inhibit metal-catalyzed oxidation. They promote tau aggregation and TPK II-mediated phosphorylation, while interaction with overexpressed HADH2 causes oxidative stress and neurotoxicity. Appicans enhance neural cell adhesion to the extracellular matrix and may regulate neurite outgrowth. Gamma-CTF and caspase-cleaved peptides (e.g., C31) strongly potentiate neuronal apoptosis.

P05067

Predicted band size: 4.4 kDa

affinity purified.

Membrane; Single-pass type I membrane protein. Membrane, clathrin-coated pit. Note=Cell surface protein that rapidly becomes internalized via clathrin-coated pits. During maturation, the immature APP (N-glycosylated in the endoplasmic reticulum) moves to the Golgi complex where complete maturation occurs (O-glycosylated and sulfated). After alpha-secretase cleavage, soluble APP is released into the extracellular space and the C-terminal is internalized to endosomes and lysosomes. Some APP accumulates in secretory transport vesicles leaving the late Golgi compartment and returns to the cell surface. Gamma-CTF(59) peptide is located to both the cytoplasm and nuclei of neurons. It can be translocated to the nucleus through association with APBB1 (Fe65). Beta-APP42 associates with FRPL1 at the cell surface and the complex is then rapidly internalized. APP sorts to the basolateral surface in epithelial cells. During neuronal differentiation, the Thr-743 phosphorylated form is located mainly in growth cones, moderately in neurites and sparingly in the cell body. Casein kinase phosphorylation can occur either at the cell surface or within a post-Golgi compartment.

Non-conjugated

Unmodified

Primary Antibody; Mouse Monoclonal Antibody

Monoclonal

Mouse

Human

Mouse, Rat

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

WB, IHC-P, IHC-F, IF-Tissue

Liquid

Supplied in 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.

Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.

Shipping with blue ice.

IgG2b

KLH conjugated synthetic peptide derived from human beta-Amyloid(1-42) aa 672-713/770 or 1-42/42