• APP Monoclonal Antibody
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Upingbio

YP-Ab-12602-10UL

APP Monoclonal Antibody

APP Monoclonal Antibody

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  • Reaction species: Human
  • Gene Name: APP
  • Protein name: Amyloid beta A4 protein, Amyloid-β, Aβ
  • Immunogen: Purified recombinant fragment of APP expressed in E. Coli.
  • Specificity: APP Monoclonal Antibody detects endogenous levels of APP protein.
  • Composition: Ascitic fluid containing 0.03% sodium azide,0.5% BSA, 50%glycerol.
  • Source: Monoclonal, Mouse
  • Dilution ratio: WB: 1/500 - 1/2000. IHC: 1/200 - 1/1000. ELISA: 1/10000.. IF 1:50-200
  • Purification process: Affinity purification
  • Storage: -20°C/1 year
  • Other Names: APP; A4; AD1; Amyloid beta A4 protein; ABPP; APPI; APP; Alzheimer disease amyloid protein; Cerebral vascular amyloid peptide; CVAP; PreA4; Protease nexin-II; PN-II
  • Background: This gene encodes a cell surface receptor and transmembrane precursor protein that is cleaved by secretases to form a number of peptides. Some of these peptides are secreted and can bind to the acetyltransferase complex APBB1/TIP60 to promote transcriptional activation, while others form the protein basis of the amyloid plaques found in the brains of patients with Alzheimer disease. In addition, two of the peptides are antimicrobial peptides, having been shown to have bacteriocidal and antifungal activities. Mutations in this gene have been implicated in autosomal dominant Alzheimer disease and cerebroarterial amyloidosis (cerebral amyloid angiopathy). Multiple transcript variants encoding several different isoforms have been found for this gene. [provided by RefSeq, Aug 2014],
  • Function: alternative products:Additional isoforms seem to exist. Experimental confirmation may be lacking for some isoforms,disease:Defects in APP are the cause of Alzheimer disease type 1 (AD1) [MIM:104300]. AD1 is a familial early-onset form of Alzheimer disease. It can be associated with cerebral amyloid angiopathy. Alzheimer disease is a neurodegenerative disorder characterized by progressive dementia, loss of cognitve abilities, and deposition of fibrillar amyloid proteins as intraneuronal neurofibrillary tangles, extracellular amyloid plaques and vascular amyloid deposits. The major constituent of these plaques is the neurotoxic amyloid-beta-APP 40-42 peptide (s), derived proteolytically from the transmembrane precursor protein APP by sequential secretase processing. The cytotoxic C-terminal fragments (CTFs) and the caspase-cleaved products such as C31 derived from APP, are also implicated
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