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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
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)
法规信息
常规特殊物品
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
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
Hyunae Kim et al.
Nutrition research (New York, N.Y.), 32(12), 956-964 (2012-12-19)
We have previously reported that dietary sericin improves epidermal dryness with the increased total Ceramide (Cer) in NC/Nga mice, an animal model of atopic dermatitis (AD). In this study, we hypothesized that the increased level of total Cer induced by
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
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