Beta-amyloid 38/Beta-APP38 Protein, Human, Recombinant (aa 672-709, His & GST)

Beta-amyloid 38/Beta-APP38 Protein, Human, Recombinant (aa 672-709, His & GST) is expressed in E. coli expression system with His and GST tag. The predicted molecular weight is 32.1 kDa and the accession number is P05067-1.

Beta-amyloid 38/Beta-APP38 Protein, Human, Recombinant (aa 672-709, His & GST)

パッケージサイズ	在庫状況	単価(税別)
100 μg	約5 days	￥ 161,000

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説明	Beta-amyloid 38/Beta-APP38 Protein, Human, Recombinant (aa 672-709, His & GST) is expressed in E. coli expression system with His and GST tag. The predicted molecular weight is 32.1 kDa and the accession number is P05067-1.

Species	Human
Expression Host	E. coli
Tag	His, GST
Accession Number	P05067-1
別名	AD1, AAA, ABETA, CVAP, PN-II, CTFgamma, Aβ, APPI, PN2, CTFγ, β-amyloid 38/β-APP38, ABPP, amyloid beta (A4) precursor protein, amyloid β (A4) precursor protein
Construction	The amino acids (Asp672-Gly709) of Human Amyloid beta A4 protein (APP770) (P05067-1), corresponding to the Beta-amyloid protein 38, was fused with the N-terminal polyhistidine-tagged GST tag at the N-terminus.
Protein Purity	> 85 % as determined by SDS-PAGE
分子量	32.1 kDa (predicted)

Endotoxin	Please contact us for more information.
Formulation	Supplied as sterile 50 mM Tris, 100 mM NaCl, 20% glycerol, 0.05% Tween 20, pH 9. 5.
Reconstitution	A Certificate of Analysis (CoA) containing reconstitution instructions is included with the products. Please refer to the CoA for detailed information.
Stability & Storage	It is recommended to store the product under sterile conditions at -20℃ to -80℃. Samples are stable for up to 12 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.
Shipping	In general, Lyophilized powders are shipping with blue ice. Solutions are shipping with dry ice.
Research 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.

参考文献

1. Grimm MO, et al. (2007) Amyloid beta as a regulator of lipid homeostasis. Trends Mol Med. 13(8): 337-44. 2. Smith EE, et al. (2009) Beta-amyloid, blood vessels, and brain function. Stroke. 40(7): 2601-6. 3. Gouras GK, et al. (2010) Intraneuronal beta-amyloid accumulation and synapse pathology in Alzheimer's disease. Acta Neuropathol. 119(5): 523-41. 4. Palop JJ, et al. (2010) Amyloid-beta-induced neuronal dysfunction in Alzheimer's disease: from synapses toward neural networks. Nat Neurosci. 13(7): 812-8.

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Beta-amyloid 38/Beta-APP38 Protein, Human, Recombinant (aa 672-709, His & GST)

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