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

Abeta 1-42 宿主: 合成
Rockland
产品编号 ABIN6699443
Supplier Product No.: 000-001-l20
发货至: 中国
  • 抗原 See all Abeta 1-42 products
    Abeta 1-42 (Amyloid beta 1-42 (Abeta 1-42))
    蛋白结构域
    AA 11-42
    资源
    • 16
    合成
    Supplier Product No.
    000-001-l20
    Supplier
    Rockland
    原理
    Beta Amyloid pyrE 11-42 Peptide
    纯度
    Greater than 95% specific peptide.
  • 应用备注

    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.

    说明

    Suggested_Applications: ELISA

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

    限制
    仅限研究用
  • 状态
    Lyophilized
    溶解方式

    Reconstitution_Buffer: Restore with deionized water (or equivalent)

    Reconstitution_Volume: 1.0 mL

    浓度
    1.0 mg/mL
    储存条件
    4 °C,-20 °C
    储存方法
    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.
    有效期
    12 months
  • 抗原
    Abeta 1-42 (Amyloid beta 1-42 (Abeta 1-42))
    背景

    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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