Amyloid beta 1-42 (Abeta 1-42) (AA 11-42) Peptid
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- Target Alle Abeta 1-42 Produkte
- Abeta 1-42 (Amyloid beta 1-42 (Abeta 1-42))
- Protein Region
- AA 11-42
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Quelle
- Synthetic
- Hersteller Produkt- Nr.
- 000-001-l20
- Hersteller
- Rockland
- Verwendungszweck
- Beta Amyloid pyrE 11-42 Peptide
- Reinheit
- Greater than 95% specific peptide.
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- Applikationshinweise
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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
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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
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- Format
- Lyophilized
- Rekonstitution
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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
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- Target
- Abeta 1-42 (Amyloid beta 1-42 (Abeta 1-42))
- Hintergrund
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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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