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  • β-Amyloid 31-35
β-Amyloid 31-35的可视化放大

β-Amyloid 31-35

β-Amyloid(31-35)是具有神经毒性的天然β淀粉样肽的最短序列。

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β-Amyloid 31-35的二维码
  • 库存: 现货
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  • 1mg
    ¥750.00
    600.00
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  • 5mg
    ¥1512.00
    1210.00
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  • 10mg
    ¥2262.00
    1810.00
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  • 货号: ajce46600
  • CAS: 149385-65-9
  • 别名: 异亮氨酰-异亮氨酰-甘氨酰-亮氨酰-蛋氨酸
  • 分子式: C25H47N5O6S
  • 分子量: 545.74
  • 纯度: >98%
  • 溶解度: Soluble in DMSO
  • 储存: Store at -20°C
  • 库存: 现货

Background

β-Amyloid (31-35) is the shortest sequence of native Amyloid-β peptide that retains neurotoxic activity.


β-Amyloid (31-35) is a functional cytotoxic domain of Aβ peptide. β-Amyloid (31-35) increases the phosphorylation of biotinylated Aβ(1-40), enhances CDK-1 activity, and also inhibits binding of Aβ to cyclin B1. β-Amyloid (31-35) is cytotoxic, and such an effect can be inhibited by olomoucine in differentiated human teratocarcinoma cell line, Ntera 2/cl-D1 (NT-2) neurons[1]. β-Amyloid (31-35) shows cytotoxic effect on cerebellar granule cells (CGC). β-Amyloid (31-35) also increases caspase-3 activity in a time-dependent manner (4-24 h) at 40 μM[2].


[1]. Milton NG, et al. The amyloid-beta peptide binds to cyclin B1 and increases human cyclin-dependent kinase-1 activity. Neurosci Lett. 2002 Apr 5;322(2):131-3. [2]. Misiti F, et al. Fragment 31-35 of beta-amyloid peptide induces neurodegeneration in rat cerebellar granule cells via bax gene expression and caspase-3 activation. A crucial role for the redox state of methionine-35 residue. Neurochem Int. 2006 Oct;49(5):525-32.

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