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Amyloid beta (A4) Precursor Protein (APP) (AA 25-35) Peptide

Rockland 000-001-l06 APP Host: Synthetic
Rockland
Catalog No. ABIN6699207
Supplier Product No.: 000-001-l06
  • Target See all APP products
    APP (Amyloid beta (A4) Precursor Protein (APP))
    Protein Region
    AA 25-35
    Source
    • 16
    Synthetic
    Supplier Product No.
    000-001-l06
    Supplier
    Rockland
    Purpose
    Beta Amyloid 25-35 Peptide
    Purity
    Greater than 95% specific peptide. [ß Amyloid 25-35-OH]
  • Application Notes

    Other: Control peptide should be used at 1.0 μg per 1.0 μL of antiserum per assay.

    Application_Note: Beta Amyloid 25-35 Control Peptide is suitable for use in ELISA, Western Blot, Dot blot, PCA, and other assays. Control peptide should be used at 1.0 μg per 1.0 μL of antiserum in per assay. Specific conditions for reactivity should be optimized by the end user.

    Restrictions
    For Research Use only
  • Format
    Lyophilized
    Reconstitution

    Reconstitution_Buffer: Restore with deionized water (or equivalent)

    Reconstitution_Volume: 1.0 mL

    Concentration
    1.0 mg/mL
    Storage
    4 °C,-20 °C
    Storage Comment
    Store vial at 2 - 8 ° C prior to opening. Aliquot contents and freeze at -20° C or below for extended storage. Avoid cycles of freezing and thawing. Centrifuge product if not completely clear after standing at room temperature. Dilute only prior to immediate use.
    Expiry Date
    12 months
  • Target
    APP (Amyloid beta (A4) Precursor Protein (APP))
    Background

    Synonyms: ABPP, APP1, Alzheimer disease amyloid protein, Cerebral vascular amyloid peptide, Protease nexin-II, control peptide, blocking peptide

    Background: Amyloid peptides, derived from amyloid precursor protein (APP), are thought to play a role in the development of the senile plaques associated with Alzheimer's disease. The amyloid hypothesis presupposes that flaws in the processing of APP result in abnormally high levels of the longer, ""stickier"" forms of beta amyloid, known as Aβ42 and Aβ43, leading to aggregation of amyloid in the neuronal cell death and ultimately neuronal death. Mutations in the structure of Aβ40 and related peptides as well as in some of the enzymes involved in the processing of APP have been shown to alter the processing of APP. The sporadic (i.e., non-genetic) form of the disease, however, is far more common, caused by aging in concert with a number of both genetic and environmental risk factors.

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