所有图片(2)
About This Item
经验公式（希尔记法）:
C6H12KNO4S
CAS号:
分子量:
233.33
MDL编号:
UNSPSC代码:
12161700
eCl@ss:
32129211
PubChem化学物质编号:
NACRES:
NA.25
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质量水平
方案
≥99% (titration)
表单
crystalline powder
有效pH范围
5.5-6.7
pKa
6.1
溶解性
water: 0.33 g/mL, clear, colorless
SMILES字符串
[K+].[O-]S(=O)(=O)CCN1CCOCC1
InChI
1S/C6H13NO4S.K/c8-12(9,10)6-3-7-1-4-11-5-2-7;/h1-6H2,(H,8,9,10);/q;+1/p-1
InChI key
IMFIKFZWLAWMQE-UHFFFAOYSA-M
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应用
MES potassium salt has been used as a component of buffers for the preparation of permeabilized fiber bundles.
生化/生理作用
MES is applicable as a Good′s buffer and is widely used in regulating the pH of reagent solutions, physiological experiments and plant culture medium.
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
个人防护装备
Eyeshields, Gloves, type N95 (US)
Tomoko Kagenishi et al.
Frontiers in plant science, 7, 79-79 (2016-03-01)
In plants, growth of roots and root hairs is regulated by the fine cellular control of pH and reactive oxygen species (ROS). MES, 2-(N-morpholino)ethanesulfonic acid as one of the Good's buffers has broadly been used for buffering medium, and it
Cody D Smith et al.
The Journal of biological chemistry, 295(48), 16207-16216 (2020-08-05)
Compensatory changes in energy expenditure occur in response to positive and negative energy balance, but the underlying mechanism remains unclear. Under low energy demand, the mitochondrial electron transport system is particularly sensitive to added energy supply (i.e. reductive stress), which
Ashley S Williams et al.
Cell metabolism, 31(1), 131-147 (2019-12-10)
This study sought to examine the functional significance of mitochondrial protein acetylation using a double knockout (DKO) mouse model harboring muscle-specific deficits in acetyl-CoA buffering and lysine deacetylation, due to genetic ablation of carnitine acetyltransferase and Sirtuin 3, respectively. DKO
Trace Thome et al.
American journal of physiology. Cell physiology, 317(4), C701-C713 (2019-07-11)
Chronic kidney disease (CKD) leads to increased skeletal muscle fatigue, weakness, and atrophy. Previous work has implicated mitochondria within the skeletal muscle as a mediator of muscle dysfunction in CKD; however, the mechanisms underlying mitochondrial dysfunction in CKD are not
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