Amyloid beta (N-term) Chicken Polyclonal Antibody

CAT#: AP31802PU-N

Amyloid beta (N-term) chicken polyclonal antibody, Aff - Purified

Product Images

Beta-Amyloid-positive neuritic plaque in cerebral cortex as seen in a post-mortum specimen taken from an Alzheimer's disease patient. Picture courtesy of Dr. Randy Woltjer, Oregon Health & Sciences University.</em>

Specifications

Product Data

• Applications: IF, IHC
• Recommended Dilution: Immunocytochemistry.
  Immunohistochemistry.
  Recommended Dilutions: 1/2000-1/5000.
  Quality Control: Antibodies were analyzed by Immunohistochemistry (at a concentration of 3 µg/ml) using Fluorescein-labeled Goat anti-Chicken IgY (1/500 dilution, Cat.-No AP31795FC-N) or HRP-labeled Goat anti-Chicken IgY (1/2000 dilution, Cat.-No AP31795HR-N) as the secondary reagent.
• Reactivities: Human, Mouse
• Host: Chicken
• Isotype: Ig
• Clonality: Polyclonal
• Immunogen: Hens were immunized with a synthetic peptide KLH conjugated corresponding to DAE FRH DSG YEV HHQ KL, residues 1-17 of the Amyloid beta-peptide (Amyloid Precursor Protein residues #672-688).
  After repeated injections, immune eggs were collected, and the IgY fractions were purified from the yolks.
• Specificity: Recognizes Beta-Amyloid Peptide (N-term).
• Formulation: 10mM PBS, pH 7.2 containing 0.02% Sodium Azide as preservative.
  State: Aff - Purified
  State: Liquid purified (filter sterilized) IgY fraction.
• Concentration: 0.1 mg/ml (based on A280 measurements).
• Purification: Affinity Chromatography using a peptide column.
• Background: Beta-Amyloid peptide is a 40- or 42-amino acid fragment of the Human Beta Amyloid Precursor Protein (770 amino acids) produced by the proteolytic actions of Beta and Gamma-secretases. Both forms of Beta-amyloid peptide are rather insoluble and tend to self-aggregate into distinctive extracellular “plaques.” These plaques are evident in brains from patients with Alzheimer’s disease, as well as in brains from individuals with a history of traumatic head injuries. In the case of Alzheimer’s disease, it has been suggested that these extracellular Beta-amyloid peptide plaques are themselves cytotoxic (rather than simply being markers of brain pathology), and are responsible for the dendritic pruning and other neurodegenerative changes seen.