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Amyloid beta 1-42 (Abeta 1-42) (AA 11-42) Peptid

Rockland 000-001-l20 Abeta 1-42 Wirt: Synthetic
Rockland
Produktnummer ABIN6699443
Hersteller Produkt- Nr.: 000-001-l20
  • Target Alle Abeta 1-42 Produkte
    Abeta 1-42 (Amyloid beta 1-42 (Abeta 1-42))
    Protein Region
    AA 11-42
    Quelle
    • 16
    Synthetic
    Hersteller Produkt- Nr.
    000-001-l20
    Hersteller
    Rockland
    Verwendungszweck
    Beta Amyloid pyrE 11-42 Peptide
    Reinheit
    Greater than 95% specific peptide.
  • Applikationshinweise

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

    Application_Note: Beta Amyloid pyrE 11-42 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.

    Kommentare

    Suggested_Applications: ELISA

    Other_Performance_Data: Control peptide should be used at 1.0 μg per 1.0 μl of antiserum per assay.

    Beschränkungen
    Nur für Forschungszwecke einsetzbar
  • Format
    Lyophilized
    Rekonstitution

    Reconstitution_Buffer: Restore with deionized water (or equivalent)

    Reconstitution_Volume: 1.0 mL

    Konzentration
    1.0 mg/mL
    Lagerung
    4 °C,-20 °C
    Informationen zur Lagerung
    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.
    Haltbarkeit
    12 months
  • Target
    Abeta 1-42 (Amyloid beta 1-42 (Abeta 1-42))
    Hintergrund

    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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