| Cat. No. |
Size |
Price |
Figures |
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RP10004-0.5 mg
| 0.5 mg | $ 114.00 | MSDS: 20080924024159 (PDF)
References:
- Richardson JS, et al. Free radicals in the neurotoxic actions of beta-amyloid. Ann N Y Acad Sci. Jan 17 1996;777:362-367.
- McLaurin J, Chakrabartty A. Characterization of the interactions of Alzheimer beta-amyloid peptides with phospholipid membranes. Eur J Biochem. Apr 15 1997;245(2):355-363.
- Hoglund K, et al. Plasma levels of beta-amyloid(1-40), beta-amyloid(1-42), and total beta-amyloid remain unaffected in adult patients with hypercholesterolemia after treatment with statins. Arch Neurol. Mar 2004;61(3):333-337.
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| Full Name | |
| Alias |
amyloid peptide; amyloid beta protein; beta amyloid plaques |
Sequence
(one-letter code) |
DAEFRHDSGYEVHHQKLVFFAEDVGSNKGAIIGLMVGGVV |
Sequence
(three-letter code) | {ASP}{ALA}{GLU}{PHE}{ARG}{HIS}{ASP}{SER}{GLY}{TYR}
{GLU}{VAL}{HIS}{HIS}{GLN}{LYS}{LEU}{VAL}{PHE}{PHE}
{ALA}{GLU}{ASP}
{VAL}{GLY}{SER}{ASN}{LYS}{GLY}{ALA}{ILE}
{ILE}{GLY}{LEU}{MET}{VAL}{GLY}{GLY}{VAL}{VAL} |
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| Description | Beta-amyloid peptide (beta-APP) is a 40-residue peptide implicated in the pathogenesis of Alzheimer’s disease (AD) and aged Down's Syndrome, which is promoted by the acquisition of an additional copy of chromosome 21. The peptide is a proteolytic product of the much larger amyloid precursor protein (APP) encoded by a gene on chromosome 21. The peptide comprises a large extracellular N-terminal domain and a short hydrophobic membrane-spanning domain, followed by a short C-terminal region. Beta-APP both precedes and forms part of the transmembrane region. |
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| Solubility | Insoluble in water, may be dissolved in any buffer of pH >9. |
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| Formula | C194H295N53O58S1 |
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| M.W. | 4329.82 |
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| Cas | 131438-79-4 |
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| Purity | > 95% |
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| Storage | Store at -20°C |
| Notes | In culture, beta-amyloid peptide is neurotrophic to undifferentiated hippocampal neurons at low concentrations and neurotoxic to mature neurons at higher concentrations. In differentiated neurons, it causes dendritic and axonal retraction followed by neuronal death. |
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