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一般描述
亮抑酶肽(Leupeptin)是水溶性和细胞渗透性有机化合物。由各种放线菌和其他多种真菌合成。
应用
亮抑酶肽已用作蛋白酶抑制剂,加入样品制备用细胞裂解缓冲液。
生化/生理作用
亮抑酶肽可用作溶酶体蛋白酶和钙蛋白酶(丝氨酸/半胱氨酸样蛋白酶)抑制剂。可抑制钙蛋白酶(calpain)过度活化引起的细胞死亡。亮抑酶肽对庆大霉素耳毒性造成的毛细胞损伤具有强保护作用。还可抑制去神经大鼠肌肉和遗传性肌营养不良症小鼠肌肉中的蛋白质降解。因此有助于防止组织萎缩。
外形
冻干。
储存及稳定性
自收到之日起,在-20ºC下保持干燥保存达18个月。 将复溶后的产品等分在-20ºC下保存长达6个月。 避免重复解冻冷冻循环。
法律信息
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
免责声明
除非我们的产品目录或产品附带的其他公司文档另有说明,否则我们的产品仅供研究使用,不得用于任何其他目的,包括但不限于未经授权的商业用途、体外诊断用途、离体或体内治疗用途或任何类型的消费或应用于人类或动物。
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
The structure and activity of leupeptins and related analogs.
K Maeda et al.
The Journal of antibiotics, 24(6), 402-404 (1971-06-01)
P Libby et al.
Science (New York, N.Y.), 199(4328), 534-536 (1978-02-03)
The protease inhibitor leupeptin decreases protein degradation in rat skeletal and cardiac muscle incubated in vitro, while protein synthesis remains unaltered. Leupeptin also lowers protein breakdown in denervated rat muscles and affected muscles from mice with hereditary muscular dystrophy. Leupeptin
Karen Maes et al.
American journal of respiratory and critical care medicine, 175(11), 1134-1138 (2007-03-24)
Controlled mechanical ventilation (CMV) has been shown to result in elevated diaphragmatic proteolysis and atrophy together with diaphragmatic contractile dysfunction. To test whether administration of leupeptin, an inhibitor of lysosomal proteases and calpain, concomitantly with 24 hours of CMV, would
Patrick J Lupardus et al.
Methods (San Diego, Calif.), 41(2), 222-231 (2006-12-27)
Our knowledge of cell cycle events such as DNA replication and mitosis has been advanced significantly through the use of Xenopus egg extracts as a model system. More recently, Xenopus extracts have been used to investigate the cellular mechanisms that
Christian Windpassinger et al.
American journal of human genetics, 101(3), 391-403 (2017-09-09)
In five separate families, we identified nine individuals affected by a previously unidentified syndrome characterized by growth retardation, spine malformation, facial dysmorphisms, and developmental delays. Using homozygosity mapping, array CGH, and exome sequencing, we uncovered bi-allelic loss-of-function CDK10 mutations segregating
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