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Amyloidβ-Peptide(10-20)(human)
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
Amyloidβ-Peptide(10-20)(human)图片
CAS NO:152286-31-2
包装与价格:
包装价格(元)
1mg电议
5mg电议
10mg电议
25mg电议

产品介绍

化学性质

Physical AppearanceA solid
StorageDesiccate at -20°C
M.Wt1446.67
Cas No.152286-31-2
FormulaC71H99N17O16
SynonymsTyr-Glu-Val-His-His-Gln-Lys-Leu-Val-Phe-Phe
Solubilityinsoluble in EtOH; ≥144.7 mg/mL in DMSO; ≥22.05 mg/mL in H2O
Chemical NameAmyloid β-Peptide (10-20) (human)
Canonical SMILESCC(C)CC(C(=O)NC(C(C)C)C(=O)NC(CC1=CC=CC=C1)C(=O)NC(CC2=CC=CC=C2)C(=O)O)NC(=O)C(CCCCN)NC(=O)C(CCC(=O)N)NC(=O)C(CC3=CN=CN3)NC(=O)C(CC4=CN=CN4)NC(=O)C(C(C)C)NC(=O)C(CCC(=O)O)NC(=O)C(CC5=CC=C(C=C5)O)N
运输条件蓝冰运输或根据您的需求运输。
一般建议为了使其更好的溶解,请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异,仅做参考。若实验所需浓度过大至产品溶解极限,请添加助溶剂助溶或自行调整浓度。溶液形式一般不宜长期储存,请尽快用完。

资料参考

在阿尔茨海默病(AD)中,β-淀粉样蛋白(Aβ)可以引发神经退行性病变 1。在非正常生理条件下,由β淀粉样前体蛋白(β-amyloid precursor protein,APP)水解产生,是一种分解代谢副产物2。

Aβ是许多不同受体和其它分子的配体3-5,通过复杂转运通路在组织和血脑屏障中运输。Aβ响应于各种不同的环境压力,能够诱导促炎活性7

可溶性β淀粉样多肽片段是明胶酶A/ IV型胶原酶/MMP-2及APP分泌酶的底物,作用于Lys16和Leu17之间,使蛋白断裂。

Figure1. Structure of Amyloid β-Peptide

 Structure of Amyloid β-Peptide

参考文献:

1. Small, D.H., Mok, S.S. & Bornstein, J.C. Alzheimer’s disease and Aβ-toxicity: From top to bottom. Nature Rev. Neurosci. 2, 595–598 (2001)

2.Soscia SJ, Kirby JE, Washicosky KJ, Tucker SM, Ingelsson M, Hyman B, Burton MA, Goldstein LE, Duong S, Tanzi RE, Moir RD (2010). Bush, Ashley I.. ed. The Alzheimer's Disease-Associated Amyloid β-Protein Is an Antimicrobial Peptide. PLoS ONE 5 (3)

3. Le Y, Gong W, Tiffany HL, Tumanov A, Nedospasov S, et al. (2001) Amyloid (b)42 activates a G-protein-coupled chemoattractant receptor, FPR-like-1.J Neurosci 21: RC123.

4. Koldamova RP, Lefterov IM, Lefterova MI, Lazo JS (2001) Apolipoprotein A-I directly interacts with amyloid precursor protein and inhibits Ab aggregation and toxicity. Biochemistry 40: 3553–3560.

5. Maezawa I, Jin LW, Woltjer RL, Maeda N, Martin GM, et al. (2004) Apolipoprotein E isoforms and apolipoprotein AI protect from amyloid precursor protein carboxy terminal fragment-associated cytotoxicity. J Neurochem 91: 1312–1321.

6. Tanzi RE, Moir RD, Wagner SL (2004) Clearance of Alzheimer’s Ab peptide: the many roads to perdition. Neuron 43: 605–608.

7. Paris D, Town T, Parker TA, Tan J, Humphrey J, et al. (1999) Inhibition of Alzheimer’s b-amyloid induced vasoactivity and proinflammatory response in microglia by a cGMP-dependent mechanism. Exp Neurol 157: 211–221.