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应用
金黄色葡萄球菌鞘氨醇酶已用于：
- 二甲胺四环素诱导大鼠皮层神经毒性的研究
- 血清样品中的鞘磷脂浓度测定
- 增强鞘磷脂酶活性，研究 PARK9 介导的外泌体生物发生
生化/生理作用
启动形成基于鞘磷脂的第二信使。激活MAPK（丝裂原活化蛋白激酶）和SAPKs（应激活化蛋白激酶）；由鞘磷脂生成神经酰胺。
细菌鞘磷脂酶在中性 pH 下具有活性。用于体外细胞培养时，它会水解质膜外叶上的鞘磷脂，并产生脂溶性神经酰胺。鞘磷脂酶是鞘磷脂酶/神经酰胺途径中的关键酶，与几种神经退行性疾病的发病机制有关。
单位定义
在pH 7.4和37℃条件下，1个单位将每分钟水解1.0 μmol TNPAL-鞘磷脂。
外形
溶于含0.25 M磷酸盐缓冲液的50%甘油，pH 7.5
储存分类代码
10 - Combustible liquids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
个人防护装备
Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)
历史批次信息供参考:
分析证书(COA)
Lot/Batch Number
其他客户在看
Taiji Tsunemi et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 34(46), 15281-15287 (2014-11-14)
Kufor-Rakeb syndrome (KRS) is caused by loss-of-function mutations in ATP13A2 (PARK9) and characterized by juvenile-onset parkinsonism, pyramidal signs, and cognitive decline. Previous studies suggested that PARK9 deficiency causes lysosomal dysfunction and α-synuclein (α-syn) accumulation, whereas PARK9 overexpression suppresses toxicity of
Measurement of sphingomyelin and ceramide cellular levels after sphingomyelinase-mediated sphingomyelin hydrolysis.
P Santana et al.
Methods in molecular biology (Clifton, N.J.), 105, 217-221 (1999-07-31)
Elin Rebecka Carlsson et al.
Frontiers in endocrinology, 9, 172-172 (2018-06-21)
Metabolic surgery is superior to lifestyle intervention in reducing weight and lowering glycemia and recently suggested as treatment for type 2 diabetes mellitus. Especially Roux-en-Y gastric bypass (RYGB) has been focus for much research, but still the mechanisms of action
Feixiang Wang et al.
The Journal of clinical investigation, 131(19) (2021-08-18)
Proper metabolic activities facilitate T cell expansion and antitumor function; however, the mechanisms underlying disruption of the T cell metabolic program and function in the tumor microenvironment (TME) remain elusive. Here, we show a zinc finger protein 91-governed (ZFP91-governed) mechanism
Ching-Min Tang et al.
Free radical biology & medicine, 50(6), 710-721 (2010-12-28)
In this study, we determined whether minocycline may protect rat cortical cultures against neurotoxicity induced by sphingomyelinase/ceramide and explored the underlying mechanisms. We found that minocycline exerted strong neuroprotective effects against toxicity induced by bacterial sphingomyelinase and synthetic C2 ceramide.
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