Amyloid beta 42 siRNA Set I(A06-911B)
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Description :Amyloid beta 42 is a pool of three individual synthetic siRNA duplexes designed to knock-down human Amyloid beta 42 mRNA expression. Each siRNA is 19-25 bases in length.
Specificity :Amyloid beta 42 siRNAs are designed to specifically knock-down human Amyloid beta 42 expression.
Formulation :The siRNAs are supplied as a lyophilized powder and shipped at room temperature.
Reconstitution Protocol :Briefly centrifuge the tubes (maximum RCF 4,000g) to collect lyophilized siRNA at the bottom of the tube. Resuspend the siRNA in 50 ul of DEPC-treated water (supplied by researcher), which results in a 1x stock solution (10 uM). Gently pipet the solution 3-5 times to mix and avoid the introduction of bubbles. Optional: aliquot 1x stock solutions for storage.
Storage and Stability :The lyophilized powder is stable for at least 4 weeks at room temperature. It is recommended that the lyophilized and resuspended siRNAs are stored at or below -20oC. After resuspension, siRNA stock solutions ≥2 uM can undergo up to 50 freeze-thaw cycles without significant degradation. For long-term storage, it is recommended that the siRNA is stored at -70oC. For most favorable performance, avoid repeated handling and multiple freeze/thaw cycles.
Format :Lyophilized powder
Gene Aliases :
Scientific 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 Abeta42 and Abeta43, leading to aggregation of amyloid in the neuronal cell death and ultimately neuronal death. Mutations in the structure of Abeta40 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.
1. Esler WP, et al: Stereochemical specificity of Alzheimer's disease beta-peptide assembly. Biopolymers. 1999 May;49(6):505-14.
2. Roher AE, et al: beta-Amyloid-(1-42) is a major component of cerebrovascular amyloid deposits: implications for the pathology of Alzheimer disease. Proc Natl Acad Sci U S A. 1993 Nov 15;90 (22):10836-40.
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Research Areas :Neurobiology