Amyloid beta (N-term) Chicken Polyclonal Antibody
CAT#: AP31802PU-N
Amyloid beta (N-term) chicken polyclonal antibody, Aff - Purified
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CNY 7688.00
货期*
                        5周
                    规格
                        Specifications
| Product Data | |
| Applications | IF, IHC | 
| Recommend 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. | 
| Reactivity | Human, Mouse | 
| Host | Chicken | 
| 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). | 
| Isotype | IgY | 
| Formulation | 10mM PBS, pH 7.2 containing 0.02% Sodium Azide as preservative. State: Aff - Purified State: Liquid purified (filter sterilized) IgY fraction. | 
| Concentration | lot specific | 
| Purification | Affinity Chromatography using a peptide column. | 
| Conjugation | Unconjugated | 
| Storage Condition | Store the antibody undiluted in the dark at 2-8°C. | 
| 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. | 
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