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文件

COO原产地证书/COA分析证书

SCP0049

[Gln²²]-Amyloid β 1-40 human

Name: [Gln<SUP>22</SUP>]-Amyloid β 1-40 human
Brand: SIGMA

≥95% (HPLC)

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所有图片(1)

About This Item

经验公式（希尔记法）:

C₁₉₄H₂₉₆N₅₄O₅₇S₁

分子量:

4328.82

分類程式碼代碼:

12352209

NACRES:

NA.77

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Sigma-Aldrich

A9810

淀粉样蛋白β蛋白片段1-42

Sigma-Aldrich

A1075

淀粉样蛋白β蛋白片段1-40

Sigma-Aldrich

H7283

Heat Shock Protein 70 human

Sigma-Aldrich

SCP0038

β 淀粉样蛋白 1-42 大鼠

Sigma-Aldrich

PP69

β-淀粉样肽（1-42），人源

Sigma-Aldrich

AG968

β 淀粉样蛋白 1-42, aβ, 超纯，HFIP，人重组

Sigma-Aldrich

596200

硫代磺素T

Sigma-Aldrich

T3516

硫代磺素T

Sigma-Aldrich

A2326

Amyloid β-Protein Fragment 40-1

Sigma-Aldrich

SCP0030

[Gly²²]-Amyloid β 1-42 Arctic human

化驗

≥95% (HPLC)

形狀

lyophilized

成份

Peptide Content, ≥70%

儲存條件

protect from light

儲存溫度

−20°C

Amino Acid Sequence

Asp-Ala-Glu-Phe-Arg-His-Asp-Ser-Gly-Tyr-Glu-Val-His-His-Gln-Lys-Leu-Val-Phe-Phe-Ala-Gln-Asp-Val-Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-Val-Gly-Gly-Val-Val

應用

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, metal binding and mechanisms of protein cross-linking in the context of diseases such as Alzheimer′s disease and neurodegeneration.

儲存類別代碼

11 - Combustible Solids

水污染物質分類（WGK）

WGK 3

閃點（°F）

Not applicable

閃點（°C）

Not applicable

分析证书(COA)

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Wild-type amyloid beta 1-40 peptide induces vascular smooth muscle cell death independently from matrix metalloprotease activity.

Régis Blaise et al.

Aging cell, 11(3), 384-393 (2012-01-21)

Cerebral amyloid angiopathy (CAA) is an important cause of intracerebral hemorrhages in the elderly, characterized by amyloid-β (Aβ) peptide accumulating in central nervous system blood vessels. Within the vessel walls, Aβ-peptide deposits [composed mainly of wild-type (WT) Aβ(1-40) peptide in

A novel approach for Aβ₁₋₄₀ quantification using immuno-PCR.

Masakazu Hashimoto et al.

Journal of neuroscience methods, 205(2), 364-367 (2012-02-14)

Several lines of evidence suggest that aggregation of the amyloid β-peptide (Aβ) in the brain is a trigger of Alzheimer's disease (AD). Thus, quantification of Aβ in several different types of samples from brain is fundamental for understanding AD pathogenesis.

Nucleotides released from Aβ₁₋₄₂ -treated microglial cells increase cell migration and Aβ₁₋₄₂ uptake through P2Y₂ receptor activation.

Hye Jung Kim et al.

Journal of neurochemistry, 121(2), 228-238 (2012-02-23)

Amyloid β-protein (Aβ) deposits in brains of Alzheimer's disease patients generate proinflammatory cytokines and chemokines that recruit microglial cells to phagocytose Aβ. Nucleotides released from apoptotic cells activate P2Y(2) receptors (P2Y(2) Rs) in macrophages to promote clearance of dead cells.

Structures of the amyloid β-peptides Aβ1-40 and Aβ1-42 as influenced by pH and a D-peptide.

Olujide O Olubiyi et al.

The journal of physical chemistry. B, 116(10), 3280-3291 (2012-02-04)

In this simulation study, we present a comparison of the secondary structure of the two major alloforms of the Alzheimer's peptide (Aβ(1-40) and Aβ(1-42)) on the basis of molecular dynamics (MD) simulations on thea microsecond time scale using the two

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[Gln²²]-Amyloid β 1-40 human