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175641

Sigma-Aldrich

Acetic anhydride-d6

99 atom % D

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About This Item

Linear Formula:
(CD3CO)2O
CAS Number:
16649-49-3
Molecular Weight:
108.13
Beilstein:
1910689
EC Number:
240-697-0
MDL number:
MFCD00044225
UNSPSC Code:
12352103
PubChem Substance ID:
24850518
NACRES:
NA.13

isotopic purity

99 atom % D

Quality Level

200

Assay

99% (CP)

form

liquid

technique(s)

protein expression: suitable

refractive index

n20/D 1.3875 (lit.)

bp

138-140 °C (lit.)

mp

-73 °C (lit.)

density

1.143 g/mL at 25 °C

mass shift

M+6

SMILES string

[2H]C([2H])([2H])C(=O)OC(=O)C([2H])([2H])[2H]

InChI

1S/C4H6O3/c1-3(5)7-4(2)6/h1-2H3/i1D3,2D3

InChI key

WFDIJRYMOXRFFG-WFGJKAKNSA-N

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Packaging

This product may be available from bulk stock and can be packaged on demand. For information on pricing, availability and packaging, please contact Stable Isotopes Customer Service.

accessory

Product No.
Description
Pricing

Signal Word

Danger

Hazard Statements

H226,H302,H314,H330

Hazard Classifications

Acute Tox. 2 Inhalation - Acute Tox. 4 Oral - Eye Dam. 1 - Flam. Liq. 3 - Skin Corr. 1B

Storage Class Code

3 - Flammable liquids

WGK

WGK 1

Flash Point(F)

120.2 °F - closed cup

Flash Point(C)

49 °C - closed cup

Certificates of Analysis (COA)

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Multiple studies have shown ribulose-1,5-bisphosphate carboxylase/oxygenase (E.C. 4.1.1.39; Rubisco) to be subject to Lys-acetylation at various residues; however, opposing reports exist about the biological significance of these post-translational modifications. One aspect of the Lys-acetylation that has not been addressed in
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Toxin-antitoxin systems in bacteria contribute to stress adaptation, dormancy, and persistence. AtaT, a type-II toxin in enterohemorrhagic E. coli, reportedly acetylates the α-amino group of the aminoacyl-moiety of initiator Met-tRNAfMet, thus inhibiting translation initiation. Here, we show that AtaT has
Chuqiao Zhang et al.
Nucleic acids research, 48(13), 7532-7544 (2020-06-06)
Escherichia coli ItaT toxin reportedly acetylates the α-amino group of the aminoacyl-moiety of Ile-tRNAIle specifically, using acetyl-CoA as an acetyl donor, thereby inhibiting protein synthesis. The mechanism of the substrate specificity of ItaT had remained elusive. Here, we present functional
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