APP (Amyloid Precursor Protein) Monoclonal Antibody (22C11), eBioscience™, Invitrogen™

Description

Description: The monoclonal antibody 22C11 recognizes human, mouse, and rat APP (Amyloid Precursor Protein). APP is expressed in high abundance in the central nervous system and has three major isoforms resulting from alternative splicing. APP plays a role in synaptic formation and repair, anterograde neuronal transport, iron export, and hormonal regulation. Secreted APP (sAPP) may have neuroprotective effects against neurotoxic insult, oxidative stress, and excitotoxicity. APP belongs to a family that contains at least two homologs, amyloid precursor-like proteins 1 and 2 (APLP1 and APLP2). Similarities between APP and APLP, especially APLP2, suggest that APLP could share and compensate for the function of APP. Proteolytic cleavage of APP results in the generation of beta amyloid, which is the primary component of senile plaques. Senile plaques are one of the major histopathologic features of Alzheimer's disease. Abnormal regulation and processing of APP also plays a role in Down's syndrome, early onset familial Alzheimer's disease, cerebral hemorrhage, and arthritis. This 22C11 antibody reacts with pre-A4 and recognizes all three isoforms of APP (immature, sAPP, and mature). This 22C11 antibody is known to cross react with APLP2. Applications Reported: This 22C11 antibody has been reported for use in microscopy, and immunocytochemistry.

Amyloid Precursor Protein (APP) or Amyloid beta precursor protein functions as a cell surface kinesin I membrane receptor, mediating the axonal transport of beta-secretase and presenilin 1. APP is important for neurite growth, neuronal adhesion and axonogenesis. APP is a 100-140 kDa transmembrane glycoprotein that exists as several isoforms resulting from alternative splicing. Proteolytic cleavage of APP by beta- and gamma-secretases results in the generation of beta amyloid, which is the primary component of senile plaques. Senile plaques are one of the major histopathologic features of Alzheimer's disease. Abnormal regulation and processing of APP also plays a role in Down's syndrome, early onset familial Alzheimer's disease, and cerebral hemorrhage.