SKU: PKSH031465-100ug-ELS
Recombinant Human Beta-amyloid 42/Beta-APP42 Protein (His & GST Tag)
Human
In Stock
RT
Specifications
| Specification | Details |
|---|---|
| Molecular Weight | 32.4 kDa |
| Tag | N-His & GST |
| Source | E.coli |
| Purity | > 80 % as determined by reducing SDS-PAGE. |
| Endotoxin Level | Please contact us for more information. |
| Format | Lyophilized from sterile PBS, 10% glycerol, pH 7.4 |
| Synonyms | AAA;ABETA;ABPP;AD1;APPI;CTFgamma;CVAP;PN-II;PN2 |
| Organism | Human |
| Accession No. | P05067-1 |
| Sequence Info | Asp672-Ala713 |
| Background | Amyloid precursor protein (APP) is a type I transmembrane protein expressed in many tissues and concentrated in the synapses of neurons; and is suggested as a regulator of synapse formation and neural plasticity. APP can be processed by two different proteolytic pathways. In one pathway; APP is cleaved by β- and γ-secretase to produce the amyloid-β-protein (Aβ; Abeta; beta-amyloid) which is the principal component of the amyloid plaques; the major pathological hallmark of Alzheimer’s disease (AD); while in the other pathway; α-secretase is involved in the cleavage of APP whose product exerts antiamyloidogenic effect and prevention of the Aβ peptide formation. The aberrant accumulation of aggregated beta-amyloid peptides (Abeta) as plaques is a hallmark of AD neuropathology and reduction of Abeta has become a leading direction of emerging experimental therapies for the disease. Besides this pathological function of Abeta; recently published data reveal that Abeta also has an essential physiological role in lipid homeostasis. Cholesterol increases Abeta production; and conversely A beta production causes a decrease in cholesterol synthesis. Abeta may be part of a mechanism controlling synaptic activity; acting as a positive regulator presynaptically and a negative regulator postsynaptically. The pathological accumulation of oligomeric Abeta assemblies depresses excitatory transmission at the synaptic level; but also triggers aberrant patterns of neuronal circuit activity and epileptiform discharges at the network level. Abeta-induced dysfunction of inhibitory interneurons likely increases synchrony among excitatory principal cells and contributes to the destabilization of neuronal networks. There is evidence that beta-amyloid can impair blood vessel function. Vascular beta-amyloid deposition; also known as cerebral amyloid angiopathy; is associated with vascular dysfunction in animal and human studies. Alzheimer disease is associated with morphological changes in capillary networks; and soluble beta-amyloid produces abnormal vascular responses to physiological and pharmacological stimuli. |
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Datasheet
Catalog Number
PKSH031465-100ug-ELS
Name
Recombinant Human Beta-amyloid 42/Beta-APP42 Protein (His & GST Tag)
Price(10000 ug)
Pack Size
10000 ug