ライフサイエンスコーパス: acetyl

1 he sn-3 position of diacylglycerol to form 3-acetyl-1,2-diacyl-sn-glycerol (acetyl-TAG).

2 The popcorn-like aroma compound 2-acetyl-1-pyrroline (2-AP) is a key contributor to the de

3 Since it was first characterised in 1983, 2-acetyl-1-pyrroline (2AP) has been considered to be the m

4 ging for preserving the key aroma compound 2-acetyl-1-pyrroline (2AP), total phenolic, and anthocyani

5 ds were methional, 2- and 3-methylbutanal, 2-acetyl-1-pyrroline and 2,3-pentanedione; whereas, in oil

6 uality fragrant varieties not only contain 2-acetyl-1-pyrroline but also several other compounds, inc

7 -furanone, 2,3-pentanedione, methional and 2-acetyl-1-pyrroline were the predominant aroma compounds.

8 Among them, compound 6c, 2-acetyl-10-((3-chloro-4-methoxybenzyl)amino)-1,2,3,4-tetr

9 0.18-1.42mg/mL suppressed the formation of 2-acetyl-2-thiazoline in model UHT milk by 32.8-63.2% afte

10 catalyzing the non-fluorescent substrate, 10-Acetyl-3,7-dihydroxyphenox-azine (ADHP), to produce high

11 tential of the acetyl-Coenzyme A precursor S-acetyl-4'-phosphopantetheine as a possible treatment for

12 ole (4-MEI), 2-methylimidazole (2-MEI) and 2-acetyl-4-tetrahydroxybutylimidazole (THI) in some foods

13 In this study, N,N'-bis (acetyl acetone) ethylenediimine (Fe3O4@SiO2-EDN) was syn

14 ions of ATP and its key negative regulators, acetyl(acyl)-CoA.

15 equires Sir2, Sir3, Sir4, nucleosomes, and O-acetyl-ADP-ribose.

16 conformational behavior of 3-O-allyl and 3-O-acetyl-alpha-d-idopyranoside derivatives complied with t

17 ynthesis offers functionalized products with acetyl and carboxyl groups in one step, in good yields,

18 ylidene-alpha-d-idopyranoside bearing allyl, acetyl, and tert-butyldiphenylsilyl (TBDPS) protecting g

19 branched/aromatic amino acids, glycoprotein acetyls, and triglycerides, and strong negative associat

20 n and aromatization reaction sequence from 3-acetyl/aroyl-2-pivaloyloxymethylindoles.

21 bazide-functionalized nopoldiol and an ortho-acetyl arylboronic acid.

22 H50Q and aS4ox are modified by DHA, whereas acetyl-aS is not.

23 oxides (aS4ox); a fully lysine-alkylated aS (acetyl-aS); and aS fibrils, testing their ability to be

24 er hippocampus levels of the neuron marker N-acetyl aspartate (NAA), along with higher levels of glut

25 rnover measured by the ratio of choline to N-acetyl-aspartate (Cho/NAA) may provide additional inform

26 late absolute metabolite concentration for N-acetyl-aspartate (NAA), choline (Cho) and creatine (Cr).

27 Ratios of N-acetyl-aspartate plus N-acetyl-aspartyl-glutamate (NAA)

28 ites, including 2-hydroxyglutaric acid and N-acetyl-aspartic acid, was also observed in the DESI mass

29 Ratios of N-acetyl-aspartate plus N-acetyl-aspartyl-glutamate (NAA) to creatine (Cr) and cho

30 els of the neurotransmitters glutamate and N-acetyl-aspartyl-glutamic acid (NAAG) and their precursor

31 quarter milk somatic cell count (SCC) and N-acetyl-beta-d-gluconaminidase (NAGase) activity data wer

32 dro-N-acetyl-beta-d-muramyl-peptide (1) to N-acetyl-beta-d-glucosamine (2) and 1,6-anhydro-N-acetyl-b

33 a and binds to two activator muropeptides, N-acetyl-beta-d-glucosamine-(1-->4)-1,6-anhydro-N-acetyl-b

34 The enzyme catalyzes hydrolysis of N-acetyl-beta-d-glucosamine-(1-->4)-1,6-anhydro-N-acetyl-b

35 Urinary albumin and N-acetyl-beta-D-glucosaminidase was significantly increase

36 tyl-beta-d-glucosamine-(1-->4)-1,6-anhydro-N-acetyl-beta-d-muramyl-l-Ala-gam ma-d-Glu-meso-DAP-d-Ala-

37 The EBD binds to the suppressor ligand UDP-N-acetyl-beta-d-muramyl-l-Ala-gamma-d-Glu-meso-DAP-d-Ala-d

38 d-Glu-meso-DAP-d-Ala-d-Ala and 1,6-anhydro-N-acetyl-beta-d-muramyl-l-Ala-gamma-d-Glu-meso-DAP-d-Ala-d

39 The EBD does not bind to 1,6-anhydro-N-acetyl-beta-d-muramyl-l-Ala-gamma-d-Glu-meso-DAP.

40 tyl-beta-d-glucosamine-(1-->4)-1,6-anhydro-N-acetyl-beta-d-muramyl-peptide (1) to N-acetyl-beta-d-glu

41 tyl-beta-d-glucosamine (2) and 1,6-anhydro-N-acetyl-beta-d-muramyl-peptide (3).

42 derivatives with inhibitory activity towards acetyl/butyrylcholinesterases and monoamine oxidases A/B

43 oxisomal targeting sequence peptide (F-PTS1, acetyl-C{K(FITC)}GGAKL) for investigating pH regulation

44 Furthermore, the full degradation of the acetyl-capped poly(potassium 3,4-dihydroxybutyrate carbo

45 f two (similar or different) substrates from acetyl carbazole proceeds via a stepwise pathway.

46 AnCDA for the first deacetylation of penta-N-acetyl-chitopentaose are 72 microM and 1.4 s(-1), respec

47 An acetyl chloride-mediated cascade transformation involvin

48 precursor for lipid biosynthesis, cytosolic acetyl CoA (Ac-CoA), is produced by ATP-citrate lyase (A

49 n chronic infection, a specific inhibitor of acetyl CoA carboxylase 1, 5-(tetradecyloxy)-2-furoic aci

50 etion and early pharmaceutical inhibition of acetyl CoA carboxylase 1, the rate limiting step of FAS,

51 largely leave out how and why ATP, NADH, and acetyl-CoA (Figure 1 ) at the molecular level play such

52 -CoA and histone acetylation levels and that acetyl-CoA abundance correlates with acetylation of spec

53 glycolytic genes and a significant delay of acetyl-CoA accumulation and reentry into growth from qui

54 proteins, alkyl hydroperoxide reductase and acetyl-CoA acetyltransferase, recognizing TPT were cruci

55 c catalytic activity and is not sensitive to acetyl-CoA activation, in contrast to other PC enzymes.

56 lyzes the formation of N-acetylagmatine from acetyl-CoA and agmatine.

57 adipose and liver, but the impact of diet on acetyl-CoA and histone acetylation in these tissues rema

58 Acly in cultured adipocytes also suppressed acetyl-CoA and histone acetylation levels.

59 he citrate-malate shuttle supplies cytosolic acetyl-CoA and plastidic glycolysis and malic enzyme sup

60 mice consuming a HFD have reduced levels of acetyl-CoA and/or acetyl-CoA:CoA ratio in these tissues.

61 uctase (rPFOR), which incorporates CO2 using acetyl-CoA as a substrate and generates pyruvate, and py

62 -CoA, crotonyl-CoA, 3-hydroxybutyryl-CoA and acetyl-CoA as observable intermediates.

63 -bound p300 HAT complexes and shows that the acetyl-CoA binding site is stably formed in the absence

64 Additional suppressor mutations in the acetyl-CoA binding site of pyruvate carboxylase (PycA) r

65 atine using an ordered sequential mechanism; acetyl-CoA binds prior to agmatine to generate an AgmNAT

66 enesis in mice by liver-specific knockout of acetyl-CoA carboxylase (ACC) genes and treat the mice wi

67 spite nutrient excess, induced both AMPK and acetyl-CoA carboxylase (ACC) phosphorylation.

68 ss is controlled by the rate-limiting enzyme acetyl-CoA carboxylase (ACC), an attractive but traditio

69 nthesis enzymes [fatty acid synthase (FASN), acetyl-CoA carboxylase (ACC), ATP citrate lyase (ACLY)].

70 AMPK phosphorylates and inhibits acetyl-CoA carboxylase (ACC), which catalyzes carboxylat

71 mRNA levels of fatty acid synthase (Fas) and acetyl-CoA carboxylase (Acc1).

72 tein content of adipose triglyceride lipase, acetyl-CoA carboxylase 2 and AMP-activated protein kinas

73 and fatty acid oxidation, activated the AMPK-acetyl-CoA carboxylase pathway, and promoted inefficient

74 s well as a protease subunit (clpP)-like and acetyl-CoA carboxylase subunit D (accD)-like open readin

75 involved in fatty acid synthesis, including acetyl-CoA carboxylase, and three out of five putative t

76 several fatty acid synthesis genes, namely, acetyl-CoA carboxylase, fatty acid synthase, SREBP1c, ch

77 le including Acc1p, the rate-limiting enzyme acetyl-CoA carboxylase.

78 nase, which results in reduction in pyruvate/acetyl-CoA conversion, mitochondrial reactive oxygen spe

79 The synthesis of acetyl-CoA depends primarily on the PDH-catalyzed conver

80 thelial cells oxidize fatty acids to produce acetyl-CoA for epigenetic modifications critical to lymp

81 tone acetylation turnover to locally produce acetyl-CoA for histone H3 acetylation in these regions a

82 PDH bypass in the cytosol, which synthesizes acetyl-CoA from acetate.

83 haea, catalyzing the reversible synthesis of acetyl-CoA from CO and a methyl group through a series o

84 ural plasticity and establish a link between acetyl-CoA generation 'on-site' at chromatin for histone

85 Acetyl-CoA has diverse fates in metabolism and can be de

86 ATP citrate-lyase produces acetyl-CoA in the nucleus and cytosol and regulates hist

87 However, how acetyl-CoA is produced under nutritional stress is uncle

88 Indeed, CR increased acetyl-CoA levels during the diauxic shift, along with e

89 Acetyl-CoA levels were decreased in the mutant.

90 A decrease in ACSS2 lowers nuclear acetyl-CoA levels, histone acetylation, and responsive e

91 ion, elevating glucose uptake, and increased acetyl-CoA levels, leading to more ROS generation in hyp

92 mide adenine dinucleotide, reduced form) and acetyl-CoA levels.

93 ation were observed with a HFD despite lower acetyl-CoA levels.

94 Our results also demonstrated that acetyl-CoA or acetyl-phosphate could acetylate MDH chemi

95 Manipulation of alternative cytosolic acetyl-CoA pathways partially decoupled lipogenesis from

96 Thus, the spatial and temporal control of acetyl-CoA production by ACLY participates in the mechan

97 ty acid-responsive factor Oaf1 in regulating acetyl-CoA production in glucose grown cells.

98 timizing the coordination of nucleocytosolic acetyl-CoA production with massive reorganization of the

99 abeling rate ( 0.03 h(-1)) of key metabolite acetyl-CoA reached to P7 strain's metabolism limitation

100 oxylic acid cycle influx of pyruvate-derived acetyl-CoA relative to beta-oxidation-derived acetyl-CoA

101 Acetyl-CoA stimulates cell growth under nutrient-limitin

102 e for the first time that CL is required for acetyl-CoA synthesis, which is decreased in CL-deficient

103 Here we show that the metabolic enzyme acetyl-CoA synthetase 2 (ACSS2) directly regulates histo

104 AMP-activated protein kinase (AMPK)-mediated acetyl-CoA synthetase 2 (ACSS2) phosphorylation at S659,

105 ular acetate levels resulting from decreased acetyl-CoA synthetase activity.

106 diauxic shift, along with expression of both acetyl-CoA synthetase genes ACS1 and ACS2 We conclude th

107 CLY) from mitochondria-derived citrate or by acetyl-CoA synthetase short-chain family member 2 (ACSS2

108 atment increased ACC levels and the ratio of acetyl-CoA to free CoA in these animals, indicating incr

109 lase (ACC), which catalyzes carboxylation of acetyl-CoA to malonyl-CoA, the first and rate-limiting r

110 lyzing the transfer of an acetyl moiety from acetyl-CoA to the C-4 amino group of UDP-d-viosamine.

111 talyzes the transfer of an acetyl group from acetyl-CoA to the sn-3 position of diacylglycerol to for

112 -limiting conditions, but how cells generate acetyl-CoA under starvation stress is less understood.

113 l enzymes that commonly produce ethanol from acetyl-CoA with acetaldehyde as intermediate and play a

114 Acetyl coenzyme A (acetyl-CoA) generated from glucose and acetate uptake is

115 Metabolic production of acetyl coenzyme A (acetyl-CoA) is linked to histone acetylation and gene re

116 on source utilization for acetyl coenzyme A (acetyl-CoA) production and gluconeogenesis.

117 ve to the availability of acetyl coenzyme A (acetyl-CoA), we investigated a role for metabolic regula

118 that A-485 competes with acetyl coenzyme A (acetyl-CoA).

119 inds prior to agmatine to generate an AgmNAT*acetyl-CoA*agmatine ternary complex prior to catalysis.

120 reversible NADH-mediated interconversions of acetyl-CoA, acetaldehyde, and ethanol but seemed to be p

121 source exhibited decreased growth, decreased acetyl-CoA, and increased intracellular acetate levels r

122 rates revealed the greatest activity against acetyl-CoA, and structure-guided mutagenesis of putative

123 cetyl-CoA relative to beta-oxidation-derived acetyl-CoA, are suggested to impact on insulin-stimulate

124 called out three metabolites: ATP, NADH, and acetyl-CoA, as sentinel molecules whose accumulation rep

125 phosphoryl transfers (ATP), acyl transfers (acetyl-CoA, carbamoyl-P), methyl transfers (SAM), prenyl

126 se or D3-acetate, which are metabolized into acetyl-coA, labeling acetyl groups through subsequent in

127 o up-regulated, leading to the production of acetyl-CoA, which can feed TAG accumulation upon exposur

128 ance for nuclear ACLY-mediated production of acetyl-CoA, which promotes histone acetylation, BRCA1 re

129 ural conformations in succinyl-CoA-bound and acetyl-CoA-bound forms.

130 The acetyl-CoA-dependent enzyme YvoF is a close relative of

131 cose carbon flow via OAA-malate-pyruvate and acetyl-CoA-fatty acid pathways in TRCs.

132 o the lipid biosynthetic precursors NADPH or acetyl-CoA.

133 hich catalyzes the conversion of pyruvate to acetyl-CoA.

134 ase (PFL) converting pyruvate to formate and acetyl-CoA.

135 n the selective binding of succinyl-CoA over acetyl-CoA.

136 ondrial matrix where it converts pyruvate to acetyl-CoA.

137 several histone lysines correlated with the acetyl-CoA: (iso)butyryl-CoA ratio in liver.

138 HFD have reduced levels of acetyl-CoA and/or acetyl-CoA:CoA ratio in these tissues.

139 zyme that catalyzes pyruvate's conversion to acetyl coenzyme A (AcCoA), thereby connecting these two

140 Acetyl coenzyme A (acetyl-CoA) generated from glucose an

141 Metabolic production of acetyl coenzyme A (acetyl-CoA) is linked to histone acet

142 an alternative carbon source utilization for acetyl coenzyme A (acetyl-CoA) production and gluconeoge

143 pair and is sensitive to the availability of acetyl coenzyme A (acetyl-CoA), we investigated a role f

144 300 and demonstrate that A-485 competes with acetyl coenzyme A (acetyl-CoA).

145 aretil (OG) is a small molecule inhibitor of acetyl coenzyme A (CoA) carboxylase (ACC), the enzyme th

146 hat the best inhibitors are competitive with acetyl coenzyme A and an X-ray cocrystal structure revea

147 leading to depletion of the energy substrate acetyl coenzyme A and the antioxidant glutathione.

148 The acetyl coenzyme A synthase (ACS) enzyme plays a central

149 a protein-based model for the NiP center of acetyl coenzyme A synthase using a nickel-substituted az

150 complex with inositol hexaphosphate (InsP6), acetyl-coenzyme A (AcCoA) and/or substrate Resistance to

151 lex stimulates the conversion of pyruvate to acetyl-coenzyme A by the pyruvate dehydrogenase complex.

152 tations in ACC2, encoding a plastid-targeted acetyl-coenzyme A carboxylase, cause hypersensitivity to

153 NDI-010976, an allosteric inhibitor of acetyl-coenzyme A carboxylases (ACC) ACC1 and ACC2, redu

154 eristics and in vivo rescue potential of the acetyl-Coenzyme A precursor S-acetyl-4'-phosphopantethei

155 pendent response to (4-hydroxy-3-nitrophenyl)acetyl conjugated to chicken gamma globulin and found a

156 Here we show that PAF increases Acetyl-CREB-binding protein (CBP/p300) histone acetyltra

157 bstrate specificity for bioorthgonal short N-acetyl cysteamine (SNAc) donors.

158 vated and the application of ROS scavenger N-acetyl cysteine (NAC) completely blocked these effects b

159 e reactive oxygen species (ROS) scavengers N-acetyl cysteine and Mito-TEMPO, we determined that mitoc

160 GSH to oxidized GSH, whereas MIOX-siRNA or N-acetyl cysteine treatment attenuated these effects.

161 nescence was prevented by the anti-oxidant N-acetyl cysteine, as well as by plumericin and PHA-408, i

162 l ankyrin-1 antagonist and the antioxidant N-acetyl cysteine.

163 y the inhibition of oxidative stress using N-acetyl cysteine.

164 prednisolone, possibly in combination with N-acetyl cysteine.

165 e effects are reversed by the anti-oxidant N-Acetyl Cysteine.

166 The anti-oxidant N-acetyl-cysteine (NAC) reduced ROS formation and decrease

167 termediate of PopP2-mediated acetylation, an acetyl-cysteine covalent adduct, lending direct support

168 n species (ROS) in podocytes and that NAC (N-acetyl-cysteine), a potent antioxidant, significantly el

169 The ROS scavenger, N-acetyl-cysteine, blocks both the mixture-induced autopha

170 exopolysaccharides both contain 1,4-linked N-acetyl-d-galactosamine and play an important role in bio

171 other sugars like N-acetyl-D-glucosamine, N-acetyl-D-galactosamine, D-glucose and D-galactose, prese

172 The monosaccharide N-acetyl-d-glucosamine (GlcNAc) is an abundant building bl

173 ansferase that modifies host proteins with N-acetyl-d-glucosamine to inhibit antibacterial and inflam

174 tivity was observed with other sugars like N-acetyl-D-glucosamine, N-acetyl-D-galactosamine, D-glucos

175 In vivo blockade of Gal-3 with N-acetyl-d-lactosamine in T. cruzi-infected mice led to a

176 Patient body fluids showed an elevation in N-acetyl-D-mannosamine levels, and patient-derived fibrobl

177 lementation with the sialic acid precursor N-acetyl-D-mannosamine restored IgG sialylation and preser

178 enalidomide, and pomalidomide, recognizes an acetyl degron of GS, resulting in ubiquitylation and deg

179 beauvericin (BEA), deoxynivalenol (DON), 15-acetyl-deoxynivalenol (15-ADON), 3-acetyl-deoxynivalenol

180 (DON), 15-acetyl-deoxynivalenol (15-ADON), 3-acetyl-deoxynivalenol (3-ADON), nivalenol (NIV), sterigm

181 , deoxynivalenol, 3-acetyldeoxynivalenol, 15-acetyl-deoxynivalenol, HT2-toxin, T2-toxin, enniatin B,

182 ver, spectroscopic measurements for the meta-acetyl derivative 3-m-OAC indicated the formation of cat

183 droxymethylaniline methyl ethers 3-5-OMe and acetyl derivatives 3-5-OAc were investigated as potentia

184 of HDAC activity, since GSNO and S-nitroso-N-acetyl-dl-penicillamine significantly and reversibly red

185 e central metabolite acetyl phosphate as the acetyl donor.

186 asymmetric hydrogenation of (E)-beta-aryl-N-acetyl enamides, for which a new C2 -symmetric phosphoru

187 O-Acetyl ester modifications of sialic acids help resist t

188 Here, we investigated O-acetyl ester removal and sialic acid degradation by Bact

189 migration to the 9-position, glycans with O-acetyl esters became susceptible to the sequential actio

190 Specifically, EstA did not act on O-acetyl esters in their initial 7-position.

191 es suggested that spontaneous migration of O-acetyl esters on the sialic acid side chain, which can o

192 essary for generation of the even pattern of acetyl esters on xylan in Arabidopsis.

193 led to high-affinity ligands (triantennary N-acetyl galactosamine = GalNAc) for hepatocyte-specific a

194 Some polypeptide N-acetyl-galactosaminyltransferases (GALNTs) are associate

195 A single human enzyme O-linked beta-N-acetyl glucosaminase (O-GlcNAcase or OGA) hydrolyzes thi

196 o OGA in O-GlcNAc regulation.O-linked beta-N-acetyl glucosamine (O-GlcNAc) is an important protein mo

197 The O-linked beta-N-acetyl glucosamine (O-GlcNAc) modification dynamically r

198 ch has revealed the involvement of a novel N-acetyl glucosamine transporter and an alpha/beta-fold hy

199 However, wheat germ agglutinin-detectable N-acetyl-glucosamine (GlcNAc) epitopes were not identified

200 blocks of HA, UDP-Glucuronic acid and UDP-N-Acetyl-Glucosamine, as well as hyaluronic acid synthase

201 -O-rhamnosyl)hexoside and quercetin-3-O-(6''-acetyl)glucosyl-2''-sinapic acid.

202 ng trimethylamine oxide (TMAO), glutamine, N-acetyl-glycoproteins, citrate, tyrosine, phenylalanine,

203 urately predicting which proteins receive an acetyl group based on their protein sequence is expected

204 ferase (EaDAcT) catalyzes the transfer of an acetyl group from acetyl-CoA to the sn-3 position of dia

205 tylase 6 (HDAC6) catalyzes the removal of an acetyl group from lysine residues of several non-histone

206 A rhodium-catalyzed intramolecular acetyl-group transfer has been achieved through a "cut a

207 There were fewer O-acetyl groups and more phosphoethanolamine and sialic ac

208 T) are two families responsible for removing acetyl groups from acetylated proteins.

209 Histone deacetylases (HDACs) remove acetyl groups from lysine residues on histone tails, pro

210 uctural features including the location of O-acetyl groups on sialic acid (SA) moieties.

211 ch are metabolized into acetyl-coA, labeling acetyl groups through subsequent incorporation into prot

212 The carboxyl, carbonyl, acetyl groups were determined in modified starches.

213 esterase (NanS) to confirm the presence of O-acetyl groups.

214 bunit is on average substituted with three O-acetyl groups.

215 thylation may lead to the decomposition of O-acetyl groups.

216 gene loci, and, as a consequence, increasing acetyl histone H3 activity and cortical neurogenesis.

217 points to monitor rates and trends of heavy acetyl incorporation.

218 (CREBBP, BAZ2B, and BRPF1b) in complex with acetyl indole derivatives reveal the influence of the ga

219 concentrations of glycosylated, malonyl, and acetyl isoflavones and a corresponding increase in the c

220 Upon autoacetylation, acetyl-K1596 (Ac-K1596) binds intramolecularly to the BR

221 Genetic suppression of N-acetyl-l-aspartate (NAA) synthesis, previously shown to

222 e enriched in oligodendroglia that cleaves N-acetyl-l-aspartate (NAA) to acetate and l-aspartic acid,

223 the putative, rapidly acting antidepressant, acetyl-l-carnitine (LAC) in the drinking water opposed t

224 gically, modulating histone acetylation with acetyl-L-carnitine (LAC) or acetyl-N-cysteine (NAC) rapi

225 mination that involves derivatization with N-acetyl-l-cysteine (NAC) and separation by HPLC was devel

226 N-acetyl-l-cysteine (NAC) exhibits protective properties i

227 the efficacy of a weak organic acid drug, N-acetyl-L-cysteine (NAC), on the eradication of biofilms

228 porting this, combinatorial treatment with N-acetyl-l-cysteine and catalase substantially inhibited t

229 Similarly, combined N-acetyl-l-cysteine and catalase treatment also suppressed

230 AlpJ, can generate these metabolites from N-acetyl-l-cysteine and l-cysteine, respectively, and that

231 rate, Lipid Mixture 1, Gelatin Peptone N3, N-Acetyl-L-Cysteine and Pluronic F-68) were assayed in ord

232 esponsive composite material consisting of N-acetyl-L-cysteine capped CdAgTe quantum dots (NAC-CdAgTe

233 with the reactive oxygen species scavenger N-acetyl-l-cysteine reduced the levels of interleukin-6, i

234 N-acetyl-L-cysteine therapy has been used in clinical stud

235 s study, we explore the effect of low dose N-acetyl-L-cysteine therapy, delivered using a targeted, s

236 Finally, administration of the antioxidant N-acetyl-l-cysteine to Ucp2(-/-) pregnant mice alleviated

237 Pretreatment with the ROS scavenger N-acetyl-L-cysteine, the ERK1/2 inhibitor UO126, or ERK1/2

238 of (-)-norlaudanosine with 1 equiv of (-)-N-acetyl-l-leucine afforded the leucinate salt (+)-13 (99:

239 state only upon genetic incorporation of N--acetyl-l-Lys (AcK), and subsequent enzymatic deacetylati

240 ar processes by catalyzing the hydrolysis of acetyl-l-lysine residues in histone and nonhistone prote

241 eucine and FMOC-l-valine, and a dipeptide, N-acetyl-l-valyl-l-leucine (N-Ac-VL), were studied via one

242 uraminic acid (Neu5Gc) content, branching, N-acetyl-lactosamine (LacNAc) extensions, and O-acetylatio

243 rising branched glycans with extended poly-N-acetyl-lactosamine (poly-LacNAc) chains, a specificity s

244 orientation of small-molecule ligands in the acetyl lysine binding site.

245 We incorporated acetyl-lysine (AcK) and the non-hydrolyzable thioacetyl-

246 rotein-protein interactions between BRD4 and acetyl-lysine has been shown to effectively block cell p

247 Acetyl-lysine modifications create docking sites for bro

248 imited understanding of BRD9 function beyond acetyl-lysine recognition.

249 omain (BET) family of chromatin adaptors and acetyl-lysine residues on chromatin has emerged as a pro

250 acetylases (HDACs) catalyze deacetylation of acetyl-lysine residues within proteins.

251 tylate and deacetyliminate Stat3 on multiple acetyl-lysine sites.

252 Bromodomains are acetyl-lysine specific protein interaction domains that

253 -azido-phenylalanine, benzoyl-phenylalanine, acetyl-lysine, and phosphoserine into selected Salmonell

254 e recently identified the YEATS domain as an acetyl-lysine-binding module, but its functional importa

255 ic domain, thereby disrupting the NAD(+) and acetyl-lysine-binding sites.

256 Here we report the discovery of the potent, acetyl-lysine-competitive, and cell active inhibitor PFI

257 in is the bromodomain (BD), which recognizes acetyl-lysines and recruits proteins to sites of acetyla

258 for the furanosylation of p-nitrophenyl 6-O-acetyl mannopyranoside.

259 attern of interactions irrespective of which acetyl mark is inserted into the pocket.

260 yltransferase, catalyzing the transfer of an acetyl moiety from acetyl-CoA to the C-4 amino group of

261 A component of this material, N-acetyl-muramic acid (NAM), serves as a core structural e

262 re successfully generated from fluorinated O-acetyl-N,O-acetal l-tartaric acid derivatives.

263 t for HABs with (11)C-PBR28 ([methyl-(11)C]N-acetyl-N-(2-methoxybenzyl)-2-phenoxy-5-pyridinamine)) (

264 acetylation with acetyl-L-carnitine (LAC) or acetyl-N-cysteine (NAC) rapidly increases xCT and activa

265 metabolites: 6-hydroxymelatonin (6-OHM), N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK), N-acetylser

266 Trimethylamine, N-acetyl neuraminic acid, 3-hydroxyisobutyrate, 3-hydroxyb

267 ESAs were similar, with a maximum of four N-acetyl-neuraminic acid (Neu5Ac) moieties detected per gl

268 damage induced by ischemia reperfusion and N-acetyl-p-aminophenol (acetaminophen) administration.

269 Acetaminophen (N-acetyl-p-aminophenol, APAP) and (13)C6-APAP were incubat

270 ioactivate APAP to the reactive metabolite N-acetyl-p-benzoquinone imine (NAPQI).

271 t convert acetaminophen to highly reactive N-acetyl-p-benzoquinone imine.

272 ssion) and increased endothelial senescence (acetyl-p53/CD31 costaining).

273 reaction (acetate + ATP [Formula: see text] acetyl phosphate + ADP), with the exception of the Entam

274 yrophosphate (PPi)/inorganic phosphate (Pi) (acetyl phosphate + Pi [Formula: see text] acetate + PPi)

275 by acetylation using the central metabolite acetyl phosphate as the acetyl donor.

276 ontaining glucose, CpxR is phosphorylated by acetyl phosphate but cannot be dephosphorylated, resulti

277 TopA is decreased by in vitro non-enzymatic acetyl phosphate mediated lysine acetylation, and the pr

278 product, glyoxylate, and increased levels of acetyl phosphate, acetoacetyl coenzyme A (acetoacetyl-Co

279 catalyzes the interconversion of acetate and acetyl phosphate, is nearly ubiquitous in bacteria but i

280 results also demonstrated that acetyl-CoA or acetyl-phosphate could acetylate MDH chemically in vitro

281 EutQ and EutP also synthesized acetyl-phosphate from ATP and acetate.

282 pyruvate oxidase, which converts pyruvate to acetyl-phosphate under non-CCR-inducing growth condition

283 een realized for the first time using chiral acetyl-protected aminomethyl oxazoline ligands.

284 nic acid), apples (rhamnitol), and onions (N-acetyl-S-(1Z)-propenyl-cysteine-sulfoxide) that can be u

285 of NAC, whereas the thiol-lacking molecule N-acetyl-S-methyl-l-cysteine failed to exert protection or

286 phylactic reaction was induced by additional acetyl-salicylic acid.

287 The major function of O-acetyl-Ser-(thiol) lyase (OAS-TL; EC 2.5.1.47) is the fo

288 es of differentially O-protected N-nitroso-N-acetyl sialyl glycosides and of isotopic labeling studie

289 the oxidative deamination of the N-nitroso-N-acetyl sialyl glycosides leading with overall retention

290 hange reactions between nitroxides with an N-acetyl substituent and oxoammonium salts with longer acy

291 rol to form 3-acetyl-1,2-diacyl-sn-glycerol (acetyl-TAG).

292 characterized acetyltransferases from other acetyl-TAG-producing plants.

293 The histone acetyl transferase GCN5 and the histone deacetylase HDA1

294 of three P450s in combination with a single acetyl transferase was identified that catalyzes the con

295 es, we show the presence of numerous choline acetyl transferase-like immunoreactive en plaque motor e

296 ypoxia result in inhibition of mTOR-mediated acetyl-transferase ARD1 S228 phosphorylation, leading to

297 etabolic rhythmicity by acting as a rhythmic acetyl-transferase for metabolic enzymes.

298 d related GCN5 bromodomain-containing lysine acetyl transferases are members of subfamily I of the br

299 The histone acetyl transferases CREB-binding protein (CBP) and its p

300 The genes encoding the histone acetyl-transferases (HATs) CREB binding protein (CREBBP)

301 exaazatriphenylene) by hydroquinone (H2Q), N-acetyl-tyrosine (N-Ac-Tyr) or guanosine-5'-monophosphate