SCP0042
[Gly35]-Amyloid β 25-35
≥95% (HPLC)
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About This Item
Prodotti consigliati
Saggio
≥95% (HPLC)
Forma fisica
lyophilized
Composizione
Peptide Content, ≥70%
Condizioni di stoccaggio
protect from light
Temperatura di conservazione
−20°C
Amino Acid Sequence
Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Gly
Applicazioni
Amyloid β (Aβ) refers to peptides derived from Amyloid precursor protein that vary in length from 36-43 amino acids. Aβ(s) peptides, their peptide fragments and mutated fragments are used to study a wide range of metabolic and regulatory functions including activation of kinases, regulation of cholesterol transport; function as a transcription factor, and regulators of inflammation. Aβ(s) peptides and their peptide fragments are also used to study oxidative stress and mechanisms of protein cross-linking in the context of diseases such as Alzheimer′s disease and neurodegeneration.
Codice della classe di stoccaggio
11 - Combustible Solids
Classe di pericolosità dell'acqua (WGK)
WGK 1
Punto d’infiammabilità (°F)
Not applicable
Punto d’infiammabilità (°C)
Not applicable
Certificati d'analisi (COA)
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Houttuyniae Herba protects rat primary cortical cells from Aμ25-35-induced neurotoxicity via regulation of calcium influx and mitochondria-mediated apoptosis.
Human & Experimental Toxicology (2012)
Current protein & peptide science, 11(1), 54-67 (2010-03-06)
Amyloid-beta (Abeta) peptide is commonly found in human Alzheimer's disease (AD) brain and is the main component of Alzheimer amyloid plaques. The predominant forms of Abeta in the human brain are Abeta(1-40) and Abeta(1-42), but Abeta(25-35) fragment, physiologically present in
Cellular and molecular neurobiology, 32(3), 353-360 (2011-11-02)
Beta-amyloid peptide (Aβ), a major protein component of senile plaques, has been considered as a critical cause in the pathogenesis of Alzheimer's disease (AD). Modulation of the Aβ-induced neurotoxicity has emerged as a possible therapeutic approach to ameliorate the onset
Neurochemical research, 37(4), 689-699 (2011-12-08)
We have investigated the neuroprotective effect of sesaminol glucosides (SG) in SK-N-SH cells. SG prevented apoptotic cell death induced by Aβ₂₅₋₃₅. In parallel, SK-N-SH cells exposed to Aβ₂₅₋₃₅ underwent oxidative stress as shown by the elevated level of intracellular ROS
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