ライフサイエンスコーパス: acetyl

1 ffectively compete with ATAD2 for the target acetyls.

2 2-Acetyl-1-pyrroline (2-AP) has been widely reported as a

3 In contrast, the concentrations of 2-acetyl-1-pyrroline in both the GBR and PGBR samples were

4 HFD, injections of the sialidase inhibitor N-acetyl-2,3-dehydro-2-deoxyneuraminic acid inhibit weight

5 he Pd-catalyzed cross-coupling reaction of 1-acetyl-2-methyl-3H-pyrrolo[2,3-c]isoquinolin-5-yl trifla

6 tabolic saccharide engineering using tetra-O-acetyl-2-N-azidoacetyl-2-deoxy-d-galactopyranose (Ac(4)G

7 models were: 2-furylmethanol, octadecanal, 2-acetyl-3-methylpyrazine, 2,3-Dihydro-3,5-dihydroxy-6-met

8 We confirmed that 9-O-acetyl, 7,9-O-acetyl, 4-O-acetyl, and Neu5Gc modifications are widely

9 Melatonin (N-acetyl-5-methoxytryptamine) is a neurohormone that maint

10 pete with the known MR1 ligands, 5-OP-RU and acetyl-6-FP, for MR1 binding and inhibit MR1-dependent M

11 We confirmed that 9-O-acetyl, 7,9-O-acetyl, 4-O-acetyl, and Neu5Gc modificatio

12 rgent and stereoselective syntheses of the N-acetyl-8a-cyanodecahydroquinoline frameworks and the bas

13 , we assessed the effects of K326Q and K328Q acetyl (Ac)-mimetic actin on Ca(2+)-dependent, in vitro

14 Herein, we present a versatile acetyl-alanine-glycine (Ac-AG) tag that conceals quantit

15 the C-terminal Lys with isotopically labeled acetyl-alanine; (3) thiol Michael addition of an isotopi

16 d heterozigosity Leu91Arg and Gly328Ser on N-acetyl-alpha-neuraminidase - 1 (NEU1) gene, underwent an

17 e chemoenzymatic synthons for synthesizing N-acetyl analogues of NmW CPS oligosaccharides containing

18 The reaction of O-acetyl analogues of these N,O-acetals with triflic acid

19 Among the identified flavonols, 8 acylates (acetyl and hydroxymethylglutaroyl) were found, of which

20 id treatment, allowing the installation of N-acetyl and N-sulfate moieties, respectively.

21 residues modified by different patterns of N-acetyl and N-sulfate moieties.

22 confirmed that 9-O-acetyl, 7,9-O-acetyl, 4-O-acetyl, and Neu5Gc modifications are widely but variably

23 ride (TFAA) makes (2-fluoroallyl)boration of acetyl arenes/hetarenes and aliphatic ketones possible w

24 Y(4)R ligands, derived from the hexapeptide acetyl-Arg-Tyr-Arg-Leu-Arg-Tyr-NH(2) (1), reported to be

25 ippocampus, tCho in hippocampus, and total N-acetyl aspartate (tNAA) in hippocampus.

26 and 48 h measurements, the rise in Lactate/N-acetyl aspartate was reduced in white (p = 0.030) and gr

27 .001); (5) glutamate-aspartate metabolism (N-acetyl aspartate: lower in AD, p = 0.002); and (6) neuro

28 on metabolism and brain health metabolites N-acetyl-aspartate and kynurenine.

29 or imaging, along with increased levels of N-acetyl-aspartate measured by (1)H-MRS; and hypomyelinati

30 The neurotransmitter N-acetyl-aspartyl-glutamate (NAAG) is the selective endoge

31 and VNN1 are reported in association with N-acetyl-aspartyl-glutamate and Linoleoyl ethanolamide, re

32 utamyl amino acids, beta-citryl-glutamate, N-acetyl-aspartyl-glutamate, and ophthalmate-a marker of g

33 sitivity C-reactive protein and glycoprotein acetyls at 3 consecutive antenatal time points, measured

34 sitivity C-reactive protein and glycoprotein acetyls at and across all 3 antenatal time points were a

35 e (GGT), alanine aminopeptidase (AAP), and N-acetyl-beta-d-glucosaminidase (NAG).

36 ococcus luteus teichuronic acid containing N-acetyl-beta-d-mannosaminuronic acid (ManNAcA).

37 nd ChIP assay demonstrated altered histone 4 acetyl binding at the TJP1 enhancer and CLDN1 enhancer a

38 measured by phloroglucinol-HCl staining, and acetyl bromide and thioacidolysis methods.

39 er the reaction of oxidized soybean oil with acetyl chloride clarified assignments of proton signals,

40 alkylation of hydrophosphorylic compounds in acetyl chloride/acetic anhydride mixture were found by (

41 re generally, based on inhibition of enzyme, acetyl cholinesterase (AChE), butyryl cholinesterase (BC

42 sis to carbon fixation through the reductive acetyl-CoA [Wood-Ljungdahl pathway (WLP)], which was int

43 growing appreciation that molecules such as acetyl-CoA act as a shared currency between metabolic fl

44 monstrated that GCBCs generate most of their acetyl-CoA and acetylcarnitine from FAs.

45 nase B-dependent manner, to regulate hepatic acetyl-CoA and cholesterol synthesis.

46 he conversion of bolus fructose into hepatic acetyl-CoA and fatty acids.

47 AMPK deletion reduced acetyl-CoA and histone acetylation, displacing BET prote

48 , the route from dietary fructose to hepatic acetyl-CoA and lipids remains unknown.

49 decreased flux of [U-(13)C]glucose to [(13)C]acetyl-CoA and M2 and M4 isotopomers of tricarboxylic ac

50 ACLY with acetyl-CoA and oxaloacetate products shows the products

51 tyl sphingosine (N-AS) is first generated by acetyl-CoA and sphingosine through SphK1.

52 he liver(4-6), in which carbon precursors of acetyl-CoA are converted into fatty acids.

53 These results identify peroxisome-derived acetyl-CoA as a key metabolic regulator of autophagy tha

54 c1(S/A) cells exhibit a reduction in acetate/acetyl-CoA availability along with elevated cellular lip

55 c environment," the hepatocyte diverted more acetyl-CoA away from lipogenesis toward ketogenesis and

56 modomain (p.Arg53His) and two at or near the acetyl-CoA binding site (p.Cys369Ser and p.Ser413Ala).

57 Preclinical and clinical data suggest that acetyl-CoA carboxylase (ACC) inhibitors have the potenti

58 phloem-mobile systemic insecticide targeting acetyl-CoA carboxylase (ACC) of pest insects and mites u

59 ) protein levels in chicken liver, activated acetyl-CoA carboxylase (ACCalpha), and increased FASN, A

60 Acetyl-CoA carboxylase (ACCase) catalyzes the first comm

61 cid synthesis (FAS) is partially mediated by acetyl-CoA carboxylase (ACCase), the first committed ste

62 nts, expresses a multicomponent, heteromeric acetyl-CoA carboxylase (htACCase), which catalyzes the g

63 Acetyl-CoA carboxylase 1 (Acc1) connects central energy

64 -limiting enzyme of fatty acid biosynthesis, acetyl-CoA carboxylase 1 (ACC1), is O-GlcNAcylated and n

65 regulatory element-binding protein [SREBP], acetyl-CoA carboxylase [ACC], peroxisome proliferator-ac

66 roptosis to AMPK-mediated phosphorylation of acetyl-CoA carboxylase and polyunsaturated fatty acid bi

67 The expression of fatty acid synthase and acetyl-CoA carboxylase involved in de novo biosynthesis

68 bserved long-term irreversible inhibition of ACETYL-COA CARBOXYLASE, and consequently FA synthesis.

69 of accD (the plastid-encoded subunit of the acetyl-CoA carboxylase, which catalyzes the first and ra

70 d state of AMPK and of its downstream target acetyl-CoA carboxylase.

71 ion in the diabetic heart, with the produced acetyl-CoA channelled into the tricarboxylic acid cycle.

72 Intracellular acetyl-CoA concentrations are associated with nutrient a

73 ride lipase, intrahepatic lipolysis, hepatic acetyl-CoA content and pyruvate carboxylase flux, while

74 Sphingosine kinase1 (SphK1) is an acetyl-CoA dependent acetyltransferase which acts on cyc

75 titative omics analyses, we demonstrate that acetyl-CoA depletion alters the integrity of the nucleol

76 r identification and quantitation of CoA and acetyl-CoA ex vivo in tissue.

77 of the nucleolus as an important hub linking acetyl-CoA fluctuations to cellular stress responses.

78 synthase homology domain in the mechanism of acetyl-CoA formation.

79 silencing of hepatic ACSS2, which generates acetyl-CoA from acetate, potently suppresses the convers

80 ased flux was secondary to greater levels of acetyl-CoA from metabolic reprogramming to beta oxidatio

81 lum (ER) acetylation machinery, transporting acetyl-CoA from the cytosol into the ER lumen where acet

82 The majority of acetyl-CoA generated by PFL was used to regenerate NAD(+

83 subset used in capsule production, while the acetyl-CoA generated by SpxB and PDHc was utilized prima

84 uted a decreased carbon flux from glucose to acetyl-CoA in the TAZ-KO cells to a ~50% decrease in pyr

85 t microbiota(9), and this supplies lipogenic acetyl-CoA independently of ACLY(10).

86 Acetyl-CoA is the substrate for de novo lipogenesis as w

87 by which a cell responds to fluctuations in acetyl-CoA levels remain elusive.

88 Time dependent studies showed that while the acetyl-CoA levels remain unaltered, CoA levels diminish

89 d proteins in the context of acutely reduced Acetyl-CoA levels under nutrient starvation.

90 Dichloroacetic acid treatment elevated acetyl-CoA levels, restored mTORC1 activation, inhibited

91 deficiency markedly lowered total cytosolic acetyl-CoA levels, which led to decreased Raptor acetyla

92 The metabolic intermediate acetyl-CoA links anabolic and catabolic processes and co

93 fructose in a manner that is independent of acetyl-CoA metabolism.

94 he Taxol biosynthetic machinery and cellular acetyl-CoA of A. terreus have been completely restored u

95 As pyruvate and acetyl-CoA play central roles in cellular metabolism, un

96 via glutamate dehydrogenase and reduction in acetyl-CoA pools, which in turn induce autophagy and cel

97 tose, pyruvate metabolism was shunted toward acetyl-CoA production.

98 CoA from the cytosol into the ER lumen where acetyl-CoA serves as the acetyl-group donor for Nepsilon

99 the active-site A cluster of wild-type (WT) Acetyl-CoA Synthase (ACS) and two variants, F229W and F2

100 s additionally implicate mTORC2 in promoting acetyl-CoA synthesis from acetate through acetyl-CoA syn

101 C2 action is controlling nuclear-cytoplasmic acetyl-CoA synthesis.

102 inctly localized acetate-activating enzymes, ACETYL-COA SYNTHETASE (ACS) in plastids and ACETATE NON-

103 ng acetyl-CoA synthesis from acetate through acetyl-CoA synthetase 2 (ACSS2).

104 ology (CSH) module, flanked by four flexible acetyl-CoA synthetase homology (ASH) domains; CoA is bou

105 .178), which transfers the acetyl group from acetyl-CoA to EctB-formed l-2,4-diaminobutyrate (DAB), y

106 They convert acetyl-CoA to ethanol via an acetaldehyde intermediate d

107 enzyme in bacterial fermentation, converting acetyl-CoA to ethanol, via two consecutive catalytic rea

108 alonate pathway in the peroxisome to convert acetyl-CoA to several commercially important monoterpene

109 manipulate the nucleo-cytoplasmic levels of acetyl-CoA using clustered regularly interspaced short p

110 Coenzyme A (CoA) and acetyl-coenzyme A (acetyl-CoA) are ubiquitous cellular molecules, which med

111 the related metabolism of acetyl-coenzyme A (acetyl-CoA) confer numerous metabolic functions, includi

112 atalyze the hydrolysis of acetyl-Coenzyme A (acetyl-CoA) in the absence of an arylamine substrate usi

113 The metabolite acetyl-coenzyme A (acetyl-CoA) serves as an essential element for a wide ra

114 oxylate is condensed with acetyl coenzyme A (acetyl-CoA) to give malate, which undergoes two oxidativ

115 LY) synthesizes cytosolic acetyl coenzyme A (acetyl-CoA), a fundamental cellular building block.

116 ynthesis) and eat it (degrade acyl chains to acetyl-CoA).

117 (ACLY) is a major source of nucleocytosolic acetyl-CoA, a fundamental building block of carbon metab

118 enzyme cleaves cytosolic citrate to generate acetyl-CoA, and is upregulated after consumption of carb

119 fluxes from glucose and palmitate to produce Acetyl-CoA, and secretion of heparan sulfate proteoglyca

120 lyase (ACL), an enzyme converting citrate to acetyl-CoA, is highly induced in the kidney of overweigh

121 ht be due to the reduction on main influx of acetyl-CoA, or downregulation of ribosome biogenesis pro

122 onstituting them in vitro in the presence of acetyl-CoA, UDP- N-acetylglucosamine, NADPH, and ATP, we

123 te oxidation and generation of mitochondrial acetyl-CoA, were used for metabolic intervention.

124 y glycine reductase to acetyl-P, and then to acetyl-CoA, which is condensed with another CO(2) to for

125 nted by increasing FAO via deletion of ACC2 (acetyl-CoA-carboxylase 2) in phenylephrine-stimulated ca

126 llular acetate and decreased accumulation of acetyl-CoA-derived intermediates of central metabolism.

127 f microbial acetate feeds lipogenic pools of acetyl-CoA.

128 ode of activity as a competitive analogue of acetyl-CoA.

129 hibited TCA cycle by reducing the amounts of Acetyl-CoA.

130 nal factors, and/or increasing the influx of Acetyl-CoA.

131 and NAD(+) and by SpxB and PDHc to generate acetyl-CoA.

132 xidative decarboxylation steps to regenerate acetyl-CoA.

133 In this cycle, glyoxylate is condensed with acetyl coenzyme A (acetyl-CoA) to give malate, which und

134 P-citrate lyase (ACLY) synthesizes cytosolic acetyl coenzyme A (acetyl-CoA), a fundamental cellular b

135 Acetate, a precursor of acetyl coenzyme A (CoA) (a product of fatty acid beta-ox

136 ed its enzyme kinetics, suggesting decreased acetyl coenzyme A binding.

137 transport into mitochondria via deletion of acetyl coenzyme A carboxylase 2 (ACC2) does not cause ca

138 , sterol regulatory element-binding protein, acetyl coenzyme A carboxylase, and fatty acid synthase.

139 glucose oxidation to fuel the production of acetyl coenzyme A, acetylation of histones and induction

140 autophagosome biogenesis via its metabolite, acetyl-coenzyme A (AcCoA).

141 Coenzyme A (CoA) and acetyl-coenzyme A (acetyl-CoA) are ubiquitous cellular m

142 Acetate and the related metabolism of acetyl-coenzyme A (acetyl-CoA) confer numerous metabolic

143 zyme but can also catalyze the hydrolysis of acetyl-Coenzyme A (acetyl-CoA) in the absence of an aryl

144 The metabolite acetyl-coenzyme A (acetyl-CoA) serves as an essential el

145 ling redirected metabolic fluxes to generate acetyl-Coenzyme A (CoA) from glucose resulting in augmen

146 e epigenome of MLL-rearranged AML by linking acetyl-coenzyme A (CoA) homeostasis to Bromodomain and E

147 rtate N-acetyltransferase (gene: Nat8l) from acetyl-coenzyme A and aspartate.

148 phate-activated protein kinase activation of acetyl-coenzyme A carboxylase (ACC) and increased lipid

149 rough two separable mechanisms: dampening of acetyl-coenzyme A-dependent carbon metabolism through hi

150 e-brain magnetic resonance spectroscopy of N-acetyl compounds, glutamate+glutamine, creatine+phosphoc

151 Abnormal levels of N-acetyl compounds, glutamate+glutamine, creatine+phosphoc

152 ity of the excitation/inhibition modulator N-acetyl cysteine (NAC) and the 5-HT(1B/1D/1F) receptor ag

153 y with O(2) (.-) , decomposing to generate N-acetyl cysteine (NAC) persulfide.

154 si-NOX2 and antioxidant N-acetyl cysteine (NAC) reversed si-TTP-induced cell apopt

155 inhibitor VAS2870 or by the ROS scavenger N-acetyl cysteine (NAC).

156 um supplemented with cystine, cysteine, or N-acetyl cysteine as the sole sulfur source.

157 Antioxidants such as simvastatin and N-acetyl cysteine improved arterial dysfunction in Jak2V61

158 ive oxygen species-quenching agent such as N-acetyl cysteine in the medium, introduction of the compl

159 by treatment of cells with a ROS scavenger N-acetyl cysteine or protease inhibitors.

160 rc phosphorylation, while ROS reduction by N-acetyl cysteine partially reversed the phosphorylation.

161 Treatment with antioxidant N-acetyl cysteine phenocopied loss of Klf9 including suppr

162 phane, sulforaphane cysteine, sulforaphane N-acetyl cysteine) and indole metabolites (ascorbigen and

163 Antioxidants including N-acetyl cysteine, apocynin, and mitotempo ameliorated End

164 ), a phenomenon blocked by the antioxidant N-acetyl cysteine.

165 were given injections of the antioxidants N-acetyl-cysteine (NAC) or manganese (III) tetrakis-(4-ben

166 Michael addition of an isotopically labeled acetyl-cysteine at the maleylated N-terminus.

167 thiols (S-nitrosoglutathione and S-nitroso-N-acetyl-d,l-penicillamine), nitric oxide, oxidized GSH, a

168 T2 encodes the Golgi-localized polypeptide N-acetyl-d-galactosamine-transferase 2 isoenzyme.

169 to either a peptide, d-biotin, BODIPY, or N-acetyl-d-galactosamine.

170 We previously identified the UDP-N-acetyl-d-galactosaminuronic acid (UDP-GalNAcA) biosynthe

171 rect labeling of B cells reactive with the N-acetyl-D-glucosamine (GlcNAc)-containing Lancefield grou

172 ent lectin and its T cell-binding partner, N-acetyl-D-glucosamine (GlcNAc).

173 ) is the only enzyme that removes O-linked N-acetyl-d-glucosamine (O-GlcNAc) from target proteins.

174 des (paCOS), consisting of beta-1,4-linked N-acetyl-d-glucosamine and d-glucosamine units, possess di

175 using a panel of Le(x) analogues in which N-acetyl-d-glucosamine, l-fucose, or d-galactose (D-Gal) a

176 d, pseudo uridine, and dodecanol (0.5 mo); N-acetyl-D-hexosamine and fumaric acid (2 mo); uric acid a

177 ice administered the sialic acid precursor N-acetyl-D-mannosamine (ManNAc).

178 d its metabolites (diaminothiazine [DIAT], N-acetyl DIAT & epoxide) and cloning was attempted in a nu

179 DIAT-responsive clones cross-reacted with N-acetyl DIAT; however, no cross-reactivity was observed b

180 onal groups (e.g., halogen, nitrile, formyl, acetyl, ester).

181 cetate-eliminating enzyme, reveals a deviant acetyl esterase fold.

182 r hand, epimerization of ortho-regioisomer 2-acetyl estrone occurred during the irradiation of 3-acet

183 estrone occurred during the irradiation of 3-acetyl estrone.

184 : 3314); Methyl eugenol (PubChem CID: 7127); Acetyl eugenol (PubChem CID: 7136); trans-Isoeugenol (Pu

185 ht alkenylbenzenes (eugenol, methyl eugenol, acetyl eugenol, trans-isoeugenol, safrole, estragole, my

186 gical products through manipulation of its N-acetyl functionality, which can be cleaved under mild co

187 nterfering RNAs conjugated to triantennary N-acetyl galactosamine (GalNAc), the ligand recognized by

188 beta-1,4-N-Acetyl-Galactosaminyltransferase 1 (B4GALNT1) encodes th

189 s that modify host protein substrates with N-acetyl glucosamine (GlcNAc) on arginine residues.

190 d underlying galactose yielding a terminal N-acetyl glucosamine.

191 higher in AD, p = 0.004); (4) urea cycle (N-acetyl glutamate: lower in AD, p < 0.001); (5) glutamate

192 taining disaccharide thioglycoside with 6- O-acetyl group as donor building blocks for the alpha-dire

193 se (EctA; EC 2.3.1.178), which transfers the acetyl group from acetyl-CoA to EctB-formed l-2,4-diamin

194 6 (HDAC6) primarily catalyzes the removal of acetyl group from the side chain of acetylated lysine re

195 and quantum chemical modeling, we show that acetyl group migration is a much more complex phenomenon

196 3)-enzymes that oppose Kac by buffering the acetyl group pool and catalyzing lysine deacetylation, r

197 staglandin (PG) synthesis by transfer of its acetyl group to a serine residue in the cyclooxygenase (

198 tif reveals that the tyrosine binds to the N-acetyl group to select for the "boat" conformation of N-

199 A deacetylase can remove the acetyl group, thereby restoring activity.

200 the ER lumen where acetyl-CoA serves as the acetyl-group donor for Nepsilon-lysine acetylation.

201 al and biological processes, the role of the acetyl groups and the complexity of their migration has

202 Acetyl groups at C4 ensure alpha-selective galactosylati

203 Hdac3 is a lysine deacetylase that removes acetyl groups from histones and additional proteins.

204 The modification of histones by acetyl groups has a key role in the regulation of chroma

205 ol resulted in the incorporation of labelled acetyl groups into gestating fetal brains.

206 urs in part through the direct deposition of acetyl groups that are derived from alcohol onto histone

207 , and the number of incorporated sulfate and acetyl groups).

208 ient protocol for on resin deprotection of O-acetyl groups.

209 ent protein attached at the N-terminus of an acetyl H3K9-specific scFv, tethered to a cyan fluorescen

210 -regulated SIRT1 levels, leading to elevated acetyl-HIF-1alpha and HIF-1alpha levels and enhanced aro

211 evels are associated with elevated levels of acetyl-HIF-1alpha, HIF-1alpha, and aromatase in breast t

212 We demonstrate that arginine, as its N-acetyl isopropyl ester, is amenable to GC analysis using

213 an unusual covalent intermediate, N-alpha-2 acetyl-l-2,4-diaminobutyrate (alpha-ADABA).

214 -2,4-diaminobutyrate (DAB), yielding N-gamma-acetyl-l-2,4-diaminobutyrate (N-gamma-ADABA), the substr

215 t the ectoine catabolic intermediate N-alpha-acetyl-l-2,4-diaminobutyric acid.

216 own reduced lactate, S-lactoylglutathione, N-acetyl-l-alanine, 2-hydroxyglutarate, and UMP levels.

217 ed elevation in the brain concentration of N-acetyl-L-aspartate (NAA) is a characteristic feature of

218 cINs could be reversed by Alpha Lipoic Acid/Acetyl-L-Carnitine (ALA/ALC) but not by other chemicals

219 Acetyl-L-carnitine (LAC), a mitochondria-boosting supple

220 ), idebenone (IDB), R-alpha-lipoic acid plus acetyl-L-carnitine (LCLA), was found on the CCO activity

221 The use of acetyl-l-carnitine for the prevention of CIPN in patient

222 ation were reversed by alpha lipoic acid and acetyl-L-carnitine treatments, which boost mitochondrial

223 eated buffaloes had higher milk l-carnitine, acetyl-l-carnitine, propionyl-l-carnitine and delta-vale

224 Pretreatment with N-acetyl-L-cysteine (NAC) and vitamin E (Trolox) were used

225 AQP3 and NOTCH1 expression, and the use of N-acetyl-L-cysteine altered NOTCH1 expression, suggesting

226 ory signaling pathways, as the antioxidant N-acetyl-l-cysteine and a Syk inhibitor differentially blo

227 N-acetyl-l-cysteine and mito-TEMPO blocked the induction o

228 enzyme was highly active with l-cysteine, N-acetyl-l-cysteine, and allyl mercaptan.

229 Thermus thermophilus HB27 encodes for, an O-acetyl-l-homoacetylserine sulfhydrylase (Oah2), a transc

230 ansacetylase MetX converts L-homoserine to O-acetyl-L-homoserine at the committed step of this pathwa

231 this enzyme performs gamma-elimination of O-acetyl-l-homoserine to generate the vinylglycine ketimin

232 Poly-N-acetyl-lactosamine (poly-LacNAc) structures are composed

233 dramatically reduced the cell surface poly-N-acetyl-lactosamine and led to hypersensitive and hyperre

234 rases involved in the biosynthesis of poly-N-acetyl-lactosamine chains.

235 Poly-N-acetyl-lactosamine is involved in the immune system in m

236 addition of the N-acetylglucosamine to the N-acetyl-lactosamine repeat as a key step of the chain elo

237 acterized B3GNTs, B3GNT2 is the major poly-N-acetyl-lactosamine synthase, and deletion of its coding

238 deacetylation of histone H3 acetyl-Lys9 vs. acetyl-Lys14 (Wu et al, 2018).

239 e preference for deacetylation of histone H3 acetyl-Lys9 vs. acetyl-Lys14 (Wu et al, 2018).

240 igenome through their ability to recognize N-acetyl lysine (KAc) post-translational modifications on

241 a, while concomitantly increasing histone H3 acetyl lysine 9 (H3K9ac) enrichment at TNF-alpha and IL-

242 the development and application of atypical acetyl-lysine (KAc) methyl mimetics to take advantage of

243 The mitochondrial acetyl-lysine landscape of DKO hearts was elevated well

244 The drug JQ1, which inhibits histone acetyl-lysine reader bromodomains, has shown promise for

245 nal domain) family of ubiquitously expressed acetyl-lysine reader proteins, plays a pivotal role as a

246 e products and the model nucleophile N-alpha-acetyl-lysine, we identified the alpha,beta-unsaturated

247 sociated protein BRD2 without involvement of acetyl-lysine-binding bromodomains and recruits BRD2 to

248 NAD(+) and NADH), and short-chain acyl-CoAs (acetyl, malonyl, succinyl, and propionyl).

249 of histone deacetylases revealed that other acetyl marks cannot compensate for H4K16ac loss in the o

250 The acetyl methyl group is lost during the reaction as metha

251 insight into how temperature and pH affects acetyl migration on manno-oligosaccharides.

252 etylation of xylan, followed by nonenzymatic acetyl migration to the O-3 position, resulting in produ

253 y be present in variant forms that include O-acetyl modifications at C-4, C-7, C-8, and C-9 positions

254 while IAV NAs were inhibited by Neu5Gc and O-acetyl modifications, there was significant variability

255 tently reduced binding to both Neu5Gc- and O-acetyl-modified Sia; however, while IAV NAs were inhibit

256 O-Acetyl moieties are the dominant backbone substituents o

257 de anchored to the antibody via the O- and N-acetyl moieties through either H-bonding or CH-pai inter

258 s of NmW CPS oligosaccharides containing 7-O-acetyl-N-acetylneuraminic acid (Neu5,7Ac(2)) and/or 9-O-

259 etylneuraminic acid (Neu5,7Ac(2)) and/or 9-O-acetyl-N-acetylneuraminic acid (Neu5,9Ac(2)).

260 derived from peracetylated derivatives of N-acetyl neuraminic acid on treatment with a mixture of so

261 nt glycans with a terminal 1,2-diol (e.g., N-acetyl-neuraminic acid and l-glycero-alpha-d-manno-hepto

262 ompensate for each other in removing de novo acetyls on H4 in vivo Proteomics of nascent chromatin an

263 torial selectivity seen on coupling of per-O-acetyl or benzyl-protected KDO donors in dichloromethane

264 ns at C-4, C-7, C-8, and C-9 positions and N-acetyl or N-glycolyl at C-5.

265 Importantly, acetyl-OTUD3 levels are inversely correlated with IFN-be

266 in D. desulfuricans by glycine reductase to acetyl-P, and then to acetyl-CoA, which is condensed wit

267 trapping acetaminophen reactive metabolite N-acetyl-p-benzoquinoneimine (NAPQI) with human glutathion

268 nduced liver injury caused by acetaminophen (acetyl-para-aminophenol [APAP]) is the main cause of acu

269 y low molecular weight phosphodonors such as acetyl phosphate and carbamoyl phosphate.

270 ions of arginine, ornithine, polyamines, and acetyl polyamines at baseline and 26 wk of intervention

271 al features between APAQ-Pd complexes and an acetyl-protected aminoethylpyridine APAPy-Pd complex str

272 cardiac muscle, as confirmed by quantitative acetyl-proteomics.

273 This work investigates the fate of ketyl and acetyl radicals produced during the photolysis (lambda >

274 The histone acetyl reader bromodomain-containing protein 4 (BRD4) is

275 RD9 acetyl switch and a shift in the pool of acetyl "reader" proteins in favor of BRD9-regulated targ

276 omain arrays and pull-down assays identified acetyl "reader" proteins that recognized CCAR2 acetylati

277 transcription or JQ-1 to inhibit binding of acetyl-reader proteins, H3K27ac foci still appeared but

278 2,2-trichlorovinyl)-L-cysteine (TCVC), and N-acetyl-S-(1,2,2-trichlorovinyl)-L-cysteine (NAcTCVC) was

279 ation by measuring its urinary metabolite, N-acetyl-S-(4-hydroxy-2-methyl-2-buten-1-yl)-l-cysteine (I

280 ion in N-AS generation, leading to decreased acetyl-S565 COX2 and SPM production.

281 e synthase (CS), synthesizes cysteine from O-acetyl serine (OAS) and sulfur in bacteria and plants.

282 O-acetyl serine sulfhydrylase (OASS), referred to as cyste

283 coronavirus S glycoproteins that engage 9-O-acetyl-sialogycans, with an architecture similar to thos

284 Here we show that N-acetyl sphingosine (N-AS) is first generated by acetyl-C

285 ead, nasolabial, and hand samples, whereas N-acetyl-sulfamethoxazole, a drug metabolite, was detected

286 Addition of acetyl-SVAFS-amide to hemolymph led to unregulated proPO

287 ane+JQ1 in combination implicated a BET/BRD9 acetyl switch and a shift in the pool of acetyl "reader"

288 N-Acetyl, -tosyl, and -alkyl substituted ortho-iodoaniline

289 sults provide insights into the mechanism of acetyl transfer in the SGNH/GDSL hydrolase family and hi

290 ifying the stress signaling and Gcn5 histone acetyl transferase and transcription factors, together a

291 to CaMKI-mediated activation of the histone-acetyl transferase CBP.

292 resence of RARalpha, RXRalpha and the lysine acetyl transferase PCAF in AGAP2 promoter.

293 as estimated by stereology) loss of choline acetyl-transferase (ChAT)-immunoreactive motoneurons whi

294 G and Tat.AG significantly increased histone acetyl-transferase activity and promoter histones H3 and

295 CKII-alpha, histone acetylation and histone acetyl-transferase modulate the increased replication of

296 cription and the recruitment of HBx, histone acetyl-transferase P300 and histone deacetylase 1 (HDAC1

297 vironmentally friendly alternatives, such as acetyl tributyl citrate (ATBC).

298 acids, fatty acid chain length, glycoprotein acetyls, tyrosine, and isoleucine and lower levels of hi

299 accompanying O-protecting groups (benzoyl vs acetyl) were evaluated, as well as the effects of trifli

300 epigenetic modifications (such as methyl and acetyl), which are critical for chromatin remodeling and