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Merck

M0895

Sigma-Aldrich

MES potassium salt

≥99% (titration)

Sinónimos:

2-(N-Morpholino)ethanesulfonic acid potassium salt, 4-Morpholineethanesulfonic acid potassium salt

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About This Item

Fórmula empírica (notación de Hill):
C6H12KNO4S
Número de CAS:
Peso molecular:
233.33
MDL number:
UNSPSC Code:
12161700
eCl@ss:
32129211
PubChem Substance ID:
NACRES:
NA.25

assay

≥99% (titration)

form

crystalline powder

useful pH range

5.5-6.7

pKa 

6.1

solubility

water: 0.33 g/mL, clear, colorless

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

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Categorías relacionadas

Application

MES potassium salt has been used as a component of buffers for the preparation of permeabilized fiber bundles.

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.

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)


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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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