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

APP Hôte: Synthetic
Rockland
N° du produit ABIN6699209
N° du produit (Fournisseur): 000-001-l08

Aperçu rapide pour Amyloid beta (A4) Precursor Protein (APP) (AA 25-35) Peptide (ABIN6699209)

Antigène

APP (Amyloid beta (A4) Precursor Protein (APP))

Source

  • 27
Synthetic
  • Protein Region

    AA 25-35

    N° du produit (Fournisseur)

    000-001-l08

    Fournisseur

    Rockland

    Fonction

    Beta Amyloid 25-35 Peptide

    Pureté

    Greater than 95% specific peptide. [β Amyloid 25-35, scrambled-amide]
  • Indications d'application

    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

    Stock

    4 °C,-20 °C

    Stockage commentaire

    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.

    Date de péremption

    12 months
  • Antigène

    APP (Amyloid beta (A4) Precursor Protein (APP))

    Sujet

    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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