ライフサイエンスコーパス: homocysteine

1 ability in swordfish (glutathione, cysteine, homocysteine).

2 the synthesis of many metabolites, including homocysteine.

3 H) from cystine and H2S from cysteine and/or homocysteine.

4 e-carbon units to regenerate methionine from homocysteine.

5 ide (H2S), from the amino acids cysteine and homocysteine.

6 re, high-sensitivity C-reactive protein, and homocysteine.

7 5), and endline (week 12) to measure plasma homocysteine.

8 olism and the liver responses to ethanol and homocysteine.

9 w diets along with water containing 0.18% DL-homocysteine.

10 an additional gene for sulfur insertion into homocysteine.

11 precursor for the cardiovascular risk factor homocysteine.

12 y lithium, or by elevation of the metabolite homocysteine.

13 H catalyzed the hydrolysis of SAH to produce homocysteine.

14 vention studies using betaine to lower blood homocysteine.

15 thiols made up of glutathione, cysteine, and homocysteine.

16 thways, including the efficient recycling of homocysteine.

17 6)A methyltransferase, bound to S-adenosyl-L-homocysteine.

18 ferentially via condensation of cysteine and homocysteine.

19 plementation is recognized as a way to lower homocysteine.

20 o form S-methyl-5-thioribose and S-ribosyl-l-homocysteine.

21 use of a single targeted metabolic outcome, homocysteine.

22 aracteristics, duration, dose, and change in homocysteine.

23 that mTOR senses low folate rather than high homocysteine.

24 ompared with 56 pmol/L), and 17% lower serum homocysteine (14.2 compared with 17.1 mumol/L).

25 gammaGT 7.9 IU/l (95% CI 4.14 to 11.65) and homocysteine 4.6 mumol/l p < 0.05 (95% CI 0.32 to 8.87)

26 0.6 mm Hg for each 1-SD unit increase in log homocysteine; 95% CI: -0.8, 1.9 mm Hg) but was positivel

27 Homocysteine, a metabolite of the methionine cycle, is a

28 TLS of the cyanylated cysteine or cyanylated homocysteine absorptions indicates that they do not enga

29 The amino acid metabolite homocysteine activates mTORC1 to inhibit autophagy and f

30 mplex with the cofactor product S-adenosyl-l-homocysteine (AdoHcy) at 2.4 angstrom resolution.

31 mplex with its cofactor product S-adenosyl-l-homocysteine (AdoHcy) at 2.8 A resolution and identify a

32 Changes in homocysteine after folate supplementation correlated wit

33 t midline and endline, adjusted for baseline homocysteine, age, and body mass index (BMI).

34 valuate serum and red blood cellular folate, homocysteine, alpha fetal protein cholesterol, triglycer

35 8 angstrom), or in complex with S-adenosyl-l-homocysteine and (S)-cis-N-methylstylopine (d (min) = 1.

36 inding sites for a zinc ion and substrates L-homocysteine and 5-methyl-tetrahydrofolate-glutamate3.

37 thase (CBS), resulting in an accumulation of homocysteine and a concomitant decrease of cystathionine

38 mine, resulting in formation of S-adenosyl-l-homocysteine and alpha-N-methylated proteins.

39 Plasma homocysteine and body composition were measured, and tol

40 The KU42 TE domain selects cysteine and homocysteine and catalyzes transthioesterification using

41 We demonstrate elevated levels of homocysteine and concomitantly reduced levels of vitamin

42 on of homocysteine from serine, and rates of homocysteine and cystathionine production were assessed.

43 ocysteine remethylation or the appearance of homocysteine and cystathionine.

44 molecular bases for the cellular toxicity of homocysteine and demonstrate that it induces the formati

45 We hypothesize that homocysteine and H2S regulate CBS and CSE expressions in

46 methylmalonic aciduria, and elevated plasma homocysteine and harbored the mutations c.1667_1668delAG

47 r vitamins B(12), B(6), and folic acid lower homocysteine and improve symptomatology and neurocogniti

48 increasing the transsulfuration intermediate homocysteine and inducing defects in optic vasculature,

49 n of S-adenosylhomocysteine to adenosine and homocysteine and is important in cell growth and the reg

50 (HC) has been implicated in AVNFH, levels of homocysteine and its associated pathway metabolites have

51 uria have markedly elevated plasma levels of homocysteine and methionine and reduced concentrations o

52 however, SAM is converted to the neurotoxin homocysteine and must be excreted or drawn back into the

53 actually functions as an OCBS and utilizes L-homocysteine and O-acetylserine (OAS) to produce cystath

54 Accumulation of homocysteine and S-adenosylhomocysteine, genome-wide DNA

55 ine (AdoMet) to glycine to form S-adenosyl-l-homocysteine and sarcosine.

56 CBS condenses homocysteine and serine to cystathionine that is then co

57 Interaction between plasma homocysteine and the MTHFR c.677C>T polymorphism is asso

58 Moreover, the decrease in homocysteine and the normalization of cysteine in PEGyla

59 lonic H2S synthesis, a 40% increase in serum homocysteine, and a phenotype similar to wild-type mice

60 n-related nutrient status by reducing plasma homocysteine, and assesses its potential future use in p

61 lipoprotein (HDL) cholesterol, higher total homocysteine, and higher body mass index (BMI)] and grea

62 four thiols (mercaptoacetic acid, cysteine, homocysteine, and N-acetyl-cysteine) were detected in th

63 sine; non-essential amino acids: glycine and homocysteine; and soluble carbohydrates: galactose, raff

64 rations of omega-3 (omega-3) fatty acids and homocysteine are associated with the development of brai

65 ow folate concentration and higher levels of homocysteine are associated with the loss of antithrombo

66 ng evidence suggests that abnormal levels of homocysteine are associated with vascular dysfunctions,

67 High plasma concentrations of homocysteine are assumed to be associated with a high ri

68 , possible deficiency on the basis of rising homocysteine as a metabolic indicator in persons >/=4 y

69 r adults by examining the increase in plasma homocysteine as the primary determinant.We provided caps

70 participants) using rs1801133 and additional homocysteine-associated SNPs as instruments.

71 idues 351-1600) in complex with S-adenosyl-l-homocysteine at 2.62A resolution.

72 oncentrations of 1-carbon metabolites (e.g., homocysteine) before flight.

73 ession models to determine the difference in homocysteine between pairs of trial arms at midline and

74 roteins (MA1821 and MA1822) are essential to homocysteine biosynthesis in a background lacking an add

75 drink powder and UNIMMAP reduced mean plasma homocysteine by 23.6% (-29.5 to -17.1) and 15.5% (-21.2

76 Likewise, allocation to B vitamins lowered homocysteine by 26% in the global cognition trials but a

77 ent with betaine produced a rapid decline of homocysteine by 50% to 70% in all 4 patients and, over 9

78 with UNIMMAP, the drink powder reduced mean homocysteine by 8.8% (-15.8 to -1.2; p = 0.025).

79 rotective gas, is endogenously produced from homocysteine by cystathionine beta synthase (CBS) and cy

80 cells undergo continuous transmethylation of homocysteine by methyltetrahydrofolate (CH(3)THF) to for

81 aMTH1-SAM (co-factor), and PaMTH1-S-adenosyl homocysteine (by-product) co-complexes refined to 2.0, 1

82 sed blood pressure is relevant because blood homocysteine can be effectively lowered by safe and inex

83 The methionine or homocysteine chain lies in the groove making a single hy

84 = 324), we measured plasma concentrations of homocysteine, choline, and betaine and genotyped them fo

85 inhibiting H3K27M peptide and a S-adenosyl-l-homocysteine cofactor.

86 OLS regression, a 1-SD unit increase in log homocysteine concentration was associated with an increa

87 In the MR analysis of ICBP data, homocysteine concentration was not associated with SBP (

88 The association of homocysteine concentration with SBP and DBP was assessed

89 HFR) C677T (rs1801133) was used as proxy for homocysteine concentration.

90 2919 participants aged >/=65 y with elevated homocysteine concentrations (12-50 mumol/L).

91 Elevated plasma homocysteine concentrations are a risk factor for osteop

92 Allocation to B vitamins lowered homocysteine concentrations by 28% in the cognitive-doma

93 uence of rs1801198 on holotranscobalamin and homocysteine concentrations in European-descent subjects

94 udy suggests that both vitamin B12 and total homocysteine concentrations may be related to accelerate

95 BC folate, serum vitamin B-12, and/or plasma homocysteine concentrations.

96 We also speculate that homocysteine, cysteine, or a related ligand could be inv

97 ecular weight thiols (glutathione, cysteine, homocysteine, cysteinylglycine, and beta-mercaptoethanol

98 n) = 1.6 angstrom), the product S-adenosyl-l-homocysteine (d (min) = 1.8 angstrom), or in complex wit

99 kin-6, C-reactive protein, fibrinogen, total homocysteine, D-dimer, factor VIII, plasmin-antiplasmin

100 Both supplements reduced homocysteine effectively and remain potential candidates

101 CDO and CSAD expression were proportional to homocysteine elevation, indicating a possible threshold

102 The generated homocysteine enabled the Hg(2+) to be removed from a hai

103 ation, apolipoprotein E e4 status, and total homocysteine, folate, and creatinine did not attenuate t

104 for the activated methyl cycle and generates homocysteine for conversion to l-methionine.

105 from homocysteine or utilize cysteine and/or homocysteine for synthesis of H2S, a signaling molecule.

106 y, we use metallized nanopores modified with homocysteine for the detection of insulin.

107 cysteine remethylation, the remethylation of homocysteine from serine, and rates of homocysteine and

108 The transsulfuration pathway, through which homocysteine from the methionine cycle provides sulfur f

109 Whether baseline homocysteine, genetic variation, sex, and diagnosis inte

110 Cysteine, homocysteine, glutathione, quercetin, albumin and tannic

111 Increasing levels of homocysteine had no effect on PHT mTOR signalling, sugge

112 dings do not corroborate the hypothesis that homocysteine has a causal role in blood pressure, especi

113 been shown to influence homocysteine levels; homocysteine has been implicated as a cataractogenic str

114 Although Homocysteine (HC) has been implicated in AVNFH, levels o

115 Here we hypothesize that homocysteine (Hcy) alters retinal endothelial cell barri

116 ective reactivity toward cysteine (Cys) over homocysteine (Hcy) and glutathione (GSH) under stoichiom

117 elevated levels of the amino acid metabolite homocysteine (Hcy) are at high risk of developing AD.

118 Homocysteine (Hcy) can induce endoplasmic reticulum (ER)

119 nation of relative H2S and cysteine (Cys) or homocysteine (Hcy) concentrations, two important metabol

120 The accumulation of homocysteine (Hcy) during chronic kidney failure (CKD) c

121 inherited disorder characterized by elevated homocysteine (Hcy) in plasma and tissues resulting from

122 Furthermore, homocysteine (Hcy) inhibited proliferation, adhesion, an

123 High level of homocysteine (Hcy) is a recognized risk factor for devel

124 High level of homocysteine (Hcy) is an AD risk factor and associates w

125 Elevated level of homocysteine (Hcy) is considered a risk factor for neuro

126 Previous studies have reported that homocysteine (Hcy) is increased in schizophrenia.

127 cy mice, Aza treatment normalized the plasma homocysteine (Hcy) level and BP.

128 Plasma homocysteine (Hcy) levels are positively correlated with

129 Elevated homocysteine (Hcy) levels double the risk of developing

130 hase (CBS) deficiency, a genetic disorder in homocysteine (Hcy) metabolism in humans, elevates plasma

131 ded by genes at 5q14 and 21q22.3 function in homocysteine (Hcy) metabolism, and index SNPs for each h

132 Accumulation of the homocysteine (Hcy) precursor S-adenosylhomocysteine (Ado

133 showed reduced levels of enzymes catalyzing homocysteine (Hcy) production and recycling, together wi

134 ridoxine-nonresponsive HCU involves lowering homocysteine (Hcy) with a methionine (Met)-restricted di

135 A high circulating level of homocysteine (Hcy), also known as hyperhomocysteinemia,

136 -fat diet is associated with elevated plasma homocysteine (Hcy), and both are linked to cancer.

137 Biothiols, such as glutathione (GSH), homocysteine (Hcy), and cysteine (Cys), coexist in biolo

138 Biothiols such as cysteine (Cys), homocysteine (Hcy), and glutathione (GSH) play crucial r

139 Biothiols, such as cysteine (Cys), homocysteine (Hcy), and glutathione (GSH), play a key ro

140 In addition, structures are presented for homocysteine (Hcy), D-Cys, thiosulfate, and azide bound

141 of protein lysine residues by the thioester homocysteine (Hcy)-thiolactone has been implicated in ca

142 for specific detection of cysteine (Cys) and homocysteine (Hcy).

143 re methionine cycle enzymes that remethylate homocysteine; hence, their malfunction leads to hyperhom

144 eceptors that mediate oscillatory control of homocysteine homeostasis in mice.

145 ession of DNMT1, MMP9, TIMP1, and S-adenosyl homocysteine hydrolase (SAHH) and upregulated methylene

146 logs of the SAH hydrolase Ahcy (S-adenosyl-L-homocysteine hydrolase [SAHH[), CG9977/dAhcyL1 and Ahcy8

147 Our analysis shows elevated homocysteine, hypoxia, coagulation, Osteoclast different

148 conclude that mild to moderate elevation of homocysteine in Cbs(+/-) mice is accompanied by progress

149 EG/SEG, supporting a possible causal role of homocysteine in EG/SEG.

150 drink powder based on determinants of plasma homocysteine in the target population and tested it in a

151 IKV NS5 protein in complex with S-adenosyl-L-homocysteine, in which the tandem methyltransferase (MTa

152 lalanine, cyanylated cysteine, or cyanylated homocysteine incorporated at different positions within

153 ri cannot utilize the other product of LuxS, homocysteine, indicating that phenotypes of luxS mutants

154 Diets containing ethanol or homocysteine induced hyperhomocysteinemia and glucose in

155 Here we show that homocysteine-induced ER protein (Herp), a protein highly

156 ic deletion of the GluN2A subunit attenuates homocysteine-induced increase in intracellular Ca(2+) Ou

157 te, the preferential role of GluN2A-NMDAR in homocysteine-induced neurotoxicity was distinctly differ

158 ontaining functional NMDAR (GluN2B-NMDAR) in homocysteine-induced neurotoxicity.

159 l role of GluN2A-NMDAR-mediated signaling in homocysteine-induced neurotoxicity.

160 ave previously identified a link between the homocysteine-induced suppression of the selenoprotein gl

161 Our previous findings have shown that homocysteine-induced, NMDAR-mediated neurotoxicity is fa

162 base-promoted intramolecular cyclization of homocysteine into Dha formed a stable cystathionine (thi

163 ents of one-carbon metabolism, remethylating homocysteine into methionine and providing methyl groups

164 An understanding of whether homocysteine is a cause or a marker of increased blood p

165 Elevated plasma homocysteine is a risk factor for Alzheimer disease, but

166 Folate B12-dependent remethylation of homocysteine is important, but less is understood about

167 Met metabolism changes, and increased plasma homocysteine is more apparent.

168 Elevated homocysteine is observed in schizophrenia and associated

169 c acid, glutamine, glycine, histidine, total homocysteine, isoleucine, kynurenine, leucine, lysine, m

170 und to be associated with elevated levels of homocysteine, known as hyperhomocysteinemia.

171 posing primary cortical neuronal cultures to homocysteine leads to a sustained low-level increase in

172 5% CI, -5.1 to 4.0 mg/dL; P = .81), or serum homocysteine level (Delta, 0.004 mg/L; 95% CI, -0.12 to

173 OR = 1.50; 95% CI = 1.01-2.23) and elevated homocysteine levels (>15 micromol/L: OR = 2.24; 95% CI =

174 B-vitamin supplementation reduced homocysteine levels (p = .003, effect size = -0.65).

175 fluence SVS risk through pathways other than homocysteine levels and downstream effects require furth

176 omisation the association among MTHFR C677T, homocysteine levels and WMH, approached, but did not rea

177 d Relevance: MTHFR polymorphism and elevated homocysteine levels contributed separately and jointly t

178 If these findings are confirmed, homocysteine levels may be a therapeutic target to reduc

179 t out another deleterious trait of disturbed homocysteine levels that could participate in the aetiol

180 possible pathway of MTHFR polymorphisms via homocysteine levels to cortical cataract.

181 lue Mountains Eye Study 2 cohort with normal homocysteine levels was 68.3 (8.1) years and 73.2 (8.5)

182 Serum homocysteine levels were assessed following standard met

183 t, the second survey serves as baseline when homocysteine levels were assessed, and 5-year incidence

184 Combined CT/TT genotypes and elevated homocysteine levels were associated with a 3-fold risk o

185 Increased total homocysteine levels were associated with faster rates of

186 ssociations of MTHFR polymorphisms and serum homocysteine levels with incident cortical cataract in a

187 rials demonstrated that despite reduction in homocysteine levels, disease outcome remained unaffected

188 ance, particularly in patients with elevated homocysteine levels, patients with affective psychosis,

189 ion, 14% of the sample had elevated baseline homocysteine levels, which was associated with greater i

190 the possible effects of cigarette smoking on homocysteine levels, with self-reported smoking and a co

191 and 73.2 (8.5) years for those with elevated homocysteine levels.

192 cortical cataract was partially mediated via homocysteine levels.

193 synthesis and significantly decreased serum homocysteine levels.

194 r blood glucose, serum cholesterol, or serum homocysteine levels.

195 PEX included blood glucose, cholesterol, and homocysteine levels; blood pressure; and cardiac morbidi

196 ) polymorphisms have been shown to influence homocysteine levels; homocysteine has been implicated as

197 Homocysteine lowering by using B vitamins had no signifi

198 for Alzheimer disease, but the relevance of homocysteine lowering to slow the rate of cognitive agin

199 xaenoic acid) modify the treatment effect of homocysteine-lowering B vitamins on brain atrophy rates

200 These findings suggest that any effect of homocysteine-lowering treatment in preventing stroke wil

201 Most homocysteine-lowering trials with folate and vitamins B6

202 high-sensitivity C-reactive protein <2 mg/L, homocysteine <10 micromol/L, N-terminal pro-brain natriu

203 tors VIII/IX/XI, fibrinogen, lipoprotein(a), homocysteine, lupus anticoagulant, anticardiolipin antib

204 Homocysteine may interact with both risk factors and pro

205 ther established the role of GluN2A-NMDAR in homocysteine-mediated sustained ERK MAPK phosphorylation

206 timing of expression of genes that regulate homocysteine metabolism and the liver responses to ethan

207 tidylcholines and methionine are involved in homocysteine metabolism and we found supporting evidence

208 cancer cases than controls and may implicate homocysteine metabolism as another causal pathway.

209 timing in expression of genes that regulate homocysteine metabolism compared with control mice.

210 vel mechanism for H2S-mediated regulation of homocysteine metabolism in cardiomyocytes, and a negativ

211 mplicated in inflammation, oxidative stress, homocysteine metabolism, and in cardiovascular disease a

212 FA plays an established role in folate and homocysteine metabolism, but the means by which it suppr

213 a novel role in promoting H2S production and homocysteine metabolism, which may have therapeutic valu

214 Here we report the binding of L-homocysteine, methionine, and several folate analogs.

215 betaine (N,N,N-trimethylglycine) via betaine-homocysteine methyltransferase (BHMT), which is expresse

216 ent methylation pathway-catalyzed by betaine-homocysteine methyltransferase (BHMT)-for establishing a

217 also found expression of the enzyme betaine homocysteine methyltransferase in cortical neurons.

218 We studied C57Bl/6J Bhmt (betaine-homocysteine methyltransferase)-null mice at age 4, 12,

219 define severe MTHFR deficiency, methionine, homocysteine, MTHFR enzyme activity in fibroblasts, or m

220 Six thiols (mercaptoacetic acid, cysteine, homocysteine, N-acetyl-cysteine, mercaptoethane-sulfonat

221 erhomocysteinemia was defined as total serum homocysteine of 12 micromol/L or greater.

222 erhomocysteinemia was defined as total serum homocysteine of 12 mumol/L or greater.

223 However, effect of H2S or homocysteine on CBS and CSE expression, and cross-talk b

224 he aim was to assess the causal influence of homocysteine on systolic and diastolic blood pressure (S

225 orrectly oriented for an in-line attack by l-homocysteine on the N(5)-methyl.

226 We show that binding of L-homocysteine or methionine results in conformational rea

227 HL1 cardiomyocytes with increasing doses of homocysteine or Na2S/GYY4137, a H2S donor, and measured

228 sulfur metabolism to cysteine synthesis from homocysteine or utilize cysteine and/or homocysteine for

229 the genetics of 1-carbon pathway metabolism, homocysteine, oxidative stress, endothelial dysfunction,

230 nthase and gamma-cystathionase (CSE) and for homocysteine persulfide synthesis from homocystine by CS

231 ylation, promoted by the accumulation of the homocysteine precursor SAH, suppresses GPx-1 expression

232 Initially, homocysteine reacts with native catalase and/or redox-ac

233 omplex with aclacinomycin T and S-adenosyl-L-homocysteine refined to 1.9-A resolution revealed that t

234 o thymidylate biosynthesis at the expense of homocysteine remethylation during folate deficiency.

235 ate synthesis occurs in the nucleus, whereas homocysteine remethylation occurs in the cytosol.

236 plementation did not affect in vivo rates of homocysteine remethylation or the appearance of homocyst

237 indicated that the thymidylate synthesis and homocysteine remethylation pathways compete for a limiti

238 erved in folate deficiency at the expense of homocysteine remethylation, but the mechanisms are unkno

239 In vivo fluxes of total homocysteine remethylation, the remethylation of homocys

240 switch from cystathionine to cysteine and/or homocysteine renders H2S synthesis by CSE responsive to

241 Expression of homocysteine-responsive endoplasmic reticulum-resident u

242 ), adenosylhomocysteinase (Achy) and betaine-homocysteine S-methyltransferase (Bhmt) mRNA and protein

243 eterodimer partner [SHP]-null mice), betaine-homocysteine S-methyltransferase (Bhmt), or both genes (

244 Taurine alleviates repression of betaine-homocysteine S-methyltransferase and significantly impro

245 Betaine-homocysteine S-methyltransferase deficiency causes incre

246 Betaine-homocysteine S-methyltransferases (BHMTs) are methionine

247 t the design and synthesis of poly(S-alkyl-L-homocysteine)s, which were found to be a new class of re

248 sence of its methyl donor product S-adenosyl-homocysteine (SAH) and its ortholog scTrm10 from Sacchar

249 sibly reflected in high levels of S-adenosyl-homocysteine (SAH) and low levels of S-adenosyl-methioni

250 NTMT1 in complex with cofactor S-adenosyl-L-homocysteine (SAH) and six substrate peptides, respectiv

251 The affinity of S-adenosyl-l-homocysteine (SAH) for SAM binding proteins was used to

252 Here, we describe a suite of S-adenosyl homocysteine (SAH) photoreactive probes and their applic

253 tive fluorescent biosensors for S-adenosyl-l-homocysteine (SAH) that provide a direct "mix and go" ac

254 m7)G0pppA1G2U3U4G5U6U7-3'), and S-adenosyl-l-homocysteine (SAH), the by-product of the methylation re

255 h is converted via methylation to S-adenosyl-homocysteine (SAH), which accumulates during aging.

256 cond SAM (SAM2) is converted to S-adenosyl-l-homocysteine (SAH).

257 uman tRNA3(Lys) and the product S-adenosyl-L-homocysteine show a dimer of heterodimers in which each

258 associated adducts were Cys34 disulfides of homocysteine that were less abundant in colorectal cance

259 arding the associations between plasma total homocysteine (tHcy) and B vitamin levels and age-related

260 linked hearing loss to elevated plasma total homocysteine (tHcy) and folate deficiency, and have show

261 ecrease of approximately 75% in plasma total homocysteine (tHcy) and normalization of cysteine concen

262 Moderately elevated plasma total homocysteine (tHcy) is a strong modifiable risk factor f

263 Elevated total plasma homocysteine (tHcy) is considered to be an independent c

264 In 148 stable RTRs, total serum homocysteine (tHcy) level, folate, serum albumin and cre

265 ls of B vitamin therapy to lower blood total homocysteine (tHcy) levels for prevention of stroke are

266 th folate status and (indirectly) with total homocysteine (tHcy) levels.

267 vious data suggest that elevated serum total homocysteine (tHcy) may be a risk factor for bone fractu

268 ntake is positively related and total plasma homocysteine (tHcy) negatively related to academic succe

269 s of vitamin B-12, holotranscobalamin, total homocysteine (tHcy), and methylmalonic acid (MMA) were m

270 ancy with the use of plasma cobalamin, total homocysteine (tHcy), and methylmalonic acid (MMA).

271 B12, folate, total homocysteine (tHcy), methionine, MMA, metabolites of 1C

272 ined by combining vitamin B-12, plasma total homocysteine (tHcy), methylmalonic acid (MMA), and holot

273 In 2SLS regression, for the same increase in homocysteine, the coefficients were -1.8 mm Hg for SBP (

274 onine synthase (MS) catalyzes methylation of homocysteine, the last step in the biosynthesis of methi

275 s in body composition.On the basis of plasma homocysteine, the NOAEL of supplemented Met intake is 46

276 -methyl-tetrahydrofolate-glutamate3 to the l-homocysteine thiol.

277 servations for the aminolysis of N-acetyl-dl-homocysteine thiolactone with n-butylamine in THF and CH

278 -methyl-tetrahydrofolate-glutamate3 to the L-homocysteine thiolate to generate methionine.

279 enes into the unprecedented S-oxygenation of homocysteine to engender the corresponding sulfenic acid

280 is capable of transferring 2 carbon atoms to homocysteine to generate the unconventional amino acid e

281 Various mechanisms link higher total homocysteine to higher insulin resistance (IR) and risk

282 onine cycle, in which folate and B12 convert homocysteine to methionine, which is in turn converted t

283 itamin B12 functions in the remethylation of homocysteine to methionine, which regenerates THF from 5

284 This enzyme catalyzes the remethylation of homocysteine to methionine, with betaine as the methyl d

285 the four DNA bases and the remethylation of homocysteine to methionine.

286 purine nucleotides and for remethylation of homocysteine to methionine.

287 BS) catalyzes the condensation of serine and homocysteine to water and cystathionine, which is then h

288 ex with its exhausted cofactor, S-adenosyl-l-homocysteine, together with mutagenesis studies and mole

289 Conversely, in the homocysteine-treated cardiomyocytes, CBS and miR-133a we

290 eased 5-methyl-THF production in response to homocysteine treatment, the knockin cell lines had high

291 evels of 5-methyl-THF and did not respond to homocysteine treatment.

292 We found that homocysteine upregulates CSE but downregulates CBS where

293 tion were assessed via questionnaires.Plasma homocysteine was elevated with the highest dose of suppl

294 folate, serum vitamin B-12, and plasma total homocysteine were determined.

295 B-12- and folate-dependent remethylation of homocysteine, which depends on methionine synthase (MS,

296 R)-hydroxyproline and proline by cysteine or homocysteine, which reduces the preorganization and ther

297 Lowering homocysteine with combined vitamin B-12 and folic acid s

298 The association of genetically increased homocysteine with DBP was not consistent across differen

299 nt enzyme that catalyzes the condensation of homocysteine with serine or with cysteine to form cystat

300 of effect modification except for change in homocysteine, with the most pronounced effects in trials