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經驗公式(希爾表示法):
C6H12KNO4S
CAS 編號:
分子量::
233.33
UNSPSC Code:
12161700
eCl@ss:
32129211
PubChem Substance ID:
NACRES:
NA.25
MDL number:
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產品名稱
MES 钾盐, ≥99% (titration)
SMILES string
[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
assay
≥99% (titration)
form
crystalline powder
useful pH range
5.5-6.7
pKa
6.1
solubility
water: 0.33 g/mL, clear, colorless
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Application
Biochem/physiol Actions
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.[3]
存儲類別/等級
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
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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