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Merck
모든 사진(1)

주요 문서

SCP0002

Sigma-Aldrich

Acetyl-Amyloid β 25-35

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About This Item

실험식(Hill 표기법):
C47H83N13O15S1
Molecular Weight:
1102.31
UNSPSC 코드:
12352202
NACRES:
NA.32

분석

≥95% (HPLC)

양식

lyophilized

구성

Peptide Content, ≥70%

저장 조건

protect from light

UniProt 수납 번호

저장 온도

−20°C

유전자 정보

human ... APP(351)

Amino Acid Sequence

Ac-Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met

일반 설명

Amyloid-β (Aβ) peptides are a major component of the senile plaques characteristic of the Alzheimer brain. It is a type- I transmembrane protein. The amyloid β precursor protein is cleaved to amyloid peptides 36-43 amino acids in length. Aβ (25-35) represents the region that aggregates during plaque formation and is a functional domain implicated in both neurotrophic and neurotoxic effects. The gene encoding amyloid-β is localized on human chromosome 21. Acetylation may improve stability in in vitro and in vivo assays.

애플리케이션

Acetyl-Amyloid β 25-35 has been used to prepare rat models with Alzheimer′s disease.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point (°F)

Not applicable

Flash Point (°C)

Not applicable


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문서 라이브러리에서 최근에 구매한 제품에 대한 문서를 찾아보세요.

문서 라이브러리 방문

Monomeric Amyloid Beta Peptide in Hexafluoroisopropanol Detected by Small Angle Neutron Scattering.
Zhang-Haagen B
PLoS ONE, 11(2), e0150267-e0150267 (2016)
Conformational Dynamics of Specific A? Oligomers Govern Their Ability To Replicate and Induce Neuronal Apoptosis.
Dean DN
Biochemistry, 55(15), 2238-2250 (2016)
Effect of yizhitongxuan decoction on learning and memory ability, Gaq/11 expression and Na(+)-K(+)-ATP enzyme activity in rat models of Alzheimer's disease.
Teng J
Journal of Traditional Chinese Medicine = Chung i Tsa Chih Ying Wen Pan / Sponsored by All-China Association of Traditional Chinese Medicine, Academy of Traditional Chinese Medicine, 34(4), 470-476 (2014)
Yili Wu et al.
Scientific reports, 6, 22460-22460 (2016-03-05)
Down syndrome (DS), caused by trisomy of chromosome 21, is one of the most common genetic disorders. Patients with DS display growth retardation and inevitably develop characteristic Alzheimer's disease (AD) neuropathology, including neurofibrillary tangles and neuritic plaques. The expression of

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