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#18584 Anti-Human Amyloidβ (N) Rabbit IgG Affinity Purify
- Intended Use:
- Research reagents
- Application:
- WB, IHC
- Package Size1:
- 100 μg
- Package Size2:
- 10 μg
- Note on Application Abbreviations
- WB:Western Blotting
- IHC:Immunohistochemistry
※ The product indicated as "Research reagents" in the column Intended Use cannot be used
for diagnostic nor any medical purpose.
※ The datasheet listed on this page is sample only. Please refer to the datasheet
enclosed in the product purchased before use.
Product Overview
Product Overview
Product Code | 18584 |
---|---|
Product Name | Anti-Human Amyloidβ (N) Rabbit IgG Affinity Purify |
Intended Use | Research reagents |
Application | WB, IHC |
Species | Human |
Immunizing antigen | Synthetic peptide of the N-terminal part of human Amyloidβ |
Purification Method | Purified with antigen peptide |
Specificity | Reacts with all of human Amyloidβ (1-40), (1-42) and (1-43) |
Package Form | Lyophilized product from PBS containing 1 % BSA and 0.05 % NaN3 |
Storage Condition | 2 - 8℃ |
Poisonous and Deleterious Substances | Applicable |
Cartagena | Not Applicable |
Package Size 1 | 100 μg |
Package Size 2 | 10 μg |
Remarks1 | The commercial use of products without our permission is prohibited. Please make sure to contact us and obtain permission. |
Product Description
Product Description
Alzheimer's disease (AD) is characterized by the presence of extracellular plaques and intracellular neurofibrillary tangles (NFTs) in the brain. The major protein component of these plaques is beta amyloid (Aβ) peptide, a 40 to 43 amino acid peptide cleaved from amyloid precursor protein by β-secretase and γ-secretase. Increased release of Aβ42 or Aβ43, both of which exibit a greater tendency to aggregate than Aβ40, occurs in individuals expressing certain genetic mutations, ApoE alleles or may involve other undiscovered factors. Many researchers theorize that it is this increased release of Aβ42/Aβ43 which leads to the abnormal deposition of Aβ and the associated neurotoxicity in the brains of affected individuals. It is also reported that a distinct Aβpeptide, AβN3pE, is deposited in senile plaques in a dominant and differential manner as compared with the standard Aβpeptide.
References
References
- Keto form of curcumin derivatives strongly binds to Aβ oligomers but not fibrils. Yanagisawa D et al. Biomaterials. 2021 Mar;270:120686.PMID: 33540171
- Istradefylline reduces memory deficits in aging mice with amyloid pathology. Orr AG et al. Neurobiol Dis. 2018 Feb;110:29-36.PMID: 29100987
- Prolonged running, not fluoxetine treatment, increases neurogenesis, but does not alter neuropathology, in the 3xTg mouse model of Alzheimer's disease. Marlatt MW et al. Randomized Controlled Trial Curr Top Behav Neurosci. 2013;15:313-40.PMID: 23670818
- Accumulation of intraneuronal Abeta correlates with ApoE4 genotype. Christensen DZ et al. Acta Neuropathol. 2010 May;119(5):555-66.PMID: 20217101
- Mechanism of docosahexaenoic acid-induced inhibition of in vitro Abeta1-42 fibrillation and Abeta1-42-induced toxicity in SH-S5Y5 cells. Hossain S et al. J Neurochem. 2009 Oct;111(2):568-79.PMID: 19686246
Note: Retrieve by PMID number in displayed by abstract: http://www.ncbi.nlm.nih.gov