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1 ability in swordfish (glutathione, cysteine, homocysteine).
2 re, high-sensitivity C-reactive protein, and homocysteine.
3 olism and the liver responses to ethanol and homocysteine.
4 that mTOR senses low folate rather than high homocysteine.
5 w diets along with water containing 0.18% DL-homocysteine.
6 an additional gene for sulfur insertion into homocysteine.
7 precursor for the cardiovascular risk factor homocysteine.
8 y lithium, or by elevation of the metabolite homocysteine.
9 H catalyzed the hydrolysis of SAH to produce homocysteine.
10 vention studies using betaine to lower blood homocysteine.
11 thiols made up of glutathione, cysteine, and homocysteine.
12 , S-methyl-5'-thioadenosine, methionine, and homocysteine.
13 rily related to the metabolism of folate and homocysteine.
14 the synthesis of many metabolites, including homocysteine.
15 H) from cystine and H2S from cysteine and/or homocysteine.
16 e-carbon units to regenerate methionine from homocysteine.
17 ide (H2S), from the amino acids cysteine and homocysteine.
18 ompared with 56 pmol/L), and 17% lower serum homocysteine (14.2 compared with 17.1 mumol/L).
19 0.6 mm Hg for each 1-SD unit increase in log homocysteine; 95% CI: -0.8, 1.9 mm Hg) but was positivel
20 tamins is confined to participants with high homocysteine (above the median, 11 micromol/L) and that,
21 TLS of the cyanylated cysteine or cyanylated homocysteine absorptions indicates that they do not enga
22                    The amino acid metabolite homocysteine activates mTORC1 to inhibit autophagy and f
23 mplex with its cofactor product S-adenosyl-l-homocysteine (AdoHcy) at 2.8 A resolution and identify a
24 ses; however, it is not known whether excess homocysteine alters retinal vasculature.
25 inding sites for a zinc ion and substrates L-homocysteine and 5-methyl-tetrahydrofolate-glutamate3.
26 thase (CBS), resulting in an accumulation of homocysteine and a concomitant decrease of cystathionine
27           Cysteine is a metabolic product of homocysteine and a precursor of the antioxidant glutathi
28 mine, resulting in formation of S-adenosyl-l-homocysteine and alpha-N-methylated proteins.
29                                       Plasma homocysteine and body composition were measured, and tol
30            We demonstrate elevated levels of homocysteine and concomitantly reduced levels of vitamin
31 on of homocysteine from serine, and rates of homocysteine and cystathionine production were assessed.
32 ocysteine remethylation or the appearance of homocysteine and cystathionine.
33 ctive was to assess the associations between homocysteine and cysteine and CRC incidence in postmenop
34                         Associations between homocysteine and cysteine and incident CRC in the Women'
35                      Extracellular levels of homocysteine and cysteine are comparable with other repo
36                                              Homocysteine and cysteine were measured by HPLC with pos
37                   The associations with both homocysteine and cysteine were significant for localized
38 molecular bases for the cellular toxicity of homocysteine and demonstrate that it induces the formati
39                          We hypothesize that homocysteine and H2S regulate CBS and CSE expressions in
40  methylmalonic aciduria, and elevated plasma homocysteine and harbored the mutations c.1667_1668delAG
41 n of S-adenosylhomocysteine to adenosine and homocysteine and is important in cell growth and the reg
42 (HC) has been implicated in AVNFH, levels of homocysteine and its associated pathway metabolites have
43 uria have markedly elevated plasma levels of homocysteine and methionine and reduced concentrations o
44  however, SAM is converted to the neurotoxin homocysteine and must be excreted or drawn back into the
45                              Accumulation of homocysteine and S-adenosylhomocysteine, genome-wide DNA
46 ine (AdoMet) to glycine to form S-adenosyl-l-homocysteine and sarcosine.
47                                CBS condenses homocysteine and serine to cystathionine that is then co
48                    Moreover, the decrease in homocysteine and the normalization of cysteine in PEGyla
49                                      Folate, homocysteine and vitamin B12 levels of children at birth
50                                      Folate, homocysteine and vitamin B12 levels of children at birth
51                  Neonatal cord blood folate, homocysteine and vitamin B12 levels were measured, and M
52 lonic H2S synthesis, a 40% increase in serum homocysteine, and a phenotype similar to wild-type mice
53 acellular levels of free reduced cysteamine, homocysteine, and cysteine from OHSCs within 25 s in a 2
54                Concentrations of cysteamine, homocysteine, and cysteine in the extracellular space of
55 ne, C-reactive protein, D-dimer, fibrinogen, homocysteine, and growth differentiation factor-15 level
56  lipoprotein (HDL) cholesterol, higher total homocysteine, and higher body mass index (BMI)] and grea
57 a concentrations of folate, cobalamin, total homocysteine, and methylmalonic acid with cognitive perf
58 t of serum and red blood cell folate, plasma homocysteine, and MTHFR 677C>T genotype and colonic tiss
59  four thiols (mercaptoacetic acid, cysteine, homocysteine, and N-acetyl-cysteine) were detected in th
60 n transsulfuration pathway thiols, including homocysteine, and serum ADMA and SDMA concentrations at
61 : cysteine, dihydrolipoic acid, glutathione, homocysteine, and thioredoxin, and in the presence of cy
62 rations of omega-3 (omega-3) fatty acids and homocysteine are associated with the development of brai
63 ng evidence suggests that abnormal levels of homocysteine are associated with vascular dysfunctions,
64                High plasma concentrations of homocysteine are assumed to be associated with a high ri
65 uiv each of 5'-deoxyadenosine and S-adenosyl-homocysteine are produced for each methylation reaction
66 , possible deficiency on the basis of rising homocysteine as a metabolic indicator in persons >/=4 y
67 r adults by examining the increase in plasma homocysteine as the primary determinant.We provided caps
68 participants) using rs1801133 and additional homocysteine-associated SNPs as instruments.
69 idues 351-1600) in complex with S-adenosyl-l-homocysteine at 2.62A resolution.
70 oncentrations of 1-carbon metabolites (e.g., homocysteine) before flight.
71 roteins (MA1821 and MA1822) are essential to homocysteine biosynthesis in a background lacking an add
72   Likewise, allocation to B vitamins lowered homocysteine by 26% in the global cognition trials but a
73 ent with betaine produced a rapid decline of homocysteine by 50% to 70% in all 4 patients and, over 9
74 rotective gas, is endogenously produced from homocysteine by cystathionine beta synthase (CBS) and cy
75 aMTH1-SAM (co-factor), and PaMTH1-S-adenosyl homocysteine (by-product) co-complexes refined to 2.0, 1
76 sed blood pressure is relevant because blood homocysteine can be effectively lowered by safe and inex
77 = 324), we measured plasma concentrations of homocysteine, choline, and betaine and genotyped them fo
78 inhibiting H3K27M peptide and a S-adenosyl-l-homocysteine cofactor.
79 od folate status and prevent the increase in homocysteine concentration that otherwise occurs in late
80  OLS regression, a 1-SD unit increase in log homocysteine concentration was associated with an increa
81             In the MR analysis of ICBP data, homocysteine concentration was not associated with SBP (
82                           The association of homocysteine concentration with SBP and DBP was assessed
83 HFR) C677T (rs1801133) was used as proxy for homocysteine concentration.
84 2919 participants aged >/=65 y with elevated homocysteine concentrations (12-50 mumol/L).
85 to identify genetic variants associated with homocysteine concentrations and risk of CAD.
86                              Elevated plasma homocysteine concentrations are a risk factor for osteop
87             Allocation to B vitamins lowered homocysteine concentrations by 28% in the cognitive-doma
88 uence of rs1801198 on holotranscobalamin and homocysteine concentrations in European-descent subjects
89 udy suggests that both vitamin B12 and total homocysteine concentrations may be related to accelerate
90 od bone mass, maternal phosphorus intake and homocysteine concentrations most-strongly predicted chil
91 d bone mass, whereas carbohydrate intake and homocysteine concentrations were associated with lower c
92 BC folate, serum vitamin B-12, and/or plasma homocysteine concentrations.
93 e chain lengths was only partly inhibited by homocysteine, consistent with multisite binding.
94 ocysteine (SAH), S-adenosylmethionine (SAM), homocysteine, cysteine, and dimethylglycine were also as
95                       We also speculate that homocysteine, cysteine, or a related ligand could be inv
96  serum ADMA and SDMA (LC-MS/MS), and thiols (homocysteine, cysteine, taurine, glutamylcysteine, total
97 ecular weight thiols (glutathione, cysteine, homocysteine, cysteinylglycine, and beta-mercaptoethanol
98 kin-6, C-reactive protein, fibrinogen, total homocysteine, D-dimer, factor VIII, plasmin-antiplasmin
99 CDO and CSAD expression were proportional to homocysteine elevation, indicating a possible threshold
100                                The generated homocysteine enabled the Hg(2+) to be removed from a hai
101    Overall, the effect of a 25% reduction in homocysteine equated to 0.02 y (95% CI: -0.10, 0.13 y) o
102 ation, apolipoprotein E e4 status, and total homocysteine, folate, and creatinine did not attenuate t
103 from homocysteine or utilize cysteine and/or homocysteine for synthesis of H2S, a signaling molecule.
104 y, we use metallized nanopores modified with homocysteine for the detection of insulin.
105       The latter donates its methyl group to homocysteine, forming methionine, which is then used for
106 cysteine remethylation, the remethylation of homocysteine from serine, and rates of homocysteine and
107  The transsulfuration pathway, through which homocysteine from the methionine cycle provides sulfur f
108                                    Cysteine, homocysteine, glutathione, quercetin, albumin and tannic
109 .46 (1.05, 2.04) for the highest quartile of homocysteine (>9.85 mumol/L) compared with the lowest qu
110                         Increasing levels of homocysteine had no effect on PHT mTOR signalling, sugge
111 dings do not corroborate the hypothesis that homocysteine has a causal role in blood pressure, especi
112 been shown to influence homocysteine levels; homocysteine has been implicated as a cataractogenic str
113                                     Although Homocysteine (HC) has been implicated in AVNFH, levels o
114                     Here we hypothesize that homocysteine (Hcy) alters retinal endothelial cell barri
115 tifies the disulfide bridge between proximal homocysteine (Hcy) and Cys as conferring much greater st
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                                 Furthermore, homocysteine (Hcy) inhibited proliferation, adhesion, an
121                                High level of homocysteine (Hcy) is a recognized risk factor for devel
122                                High level of homocysteine (Hcy) is an AD risk factor and associates w
123                            Elevated level of homocysteine (Hcy) is considered a risk factor for neuro
124 cy mice, Aza treatment normalized the plasma homocysteine (Hcy) level and BP.
125                                       Plasma homocysteine (Hcy) levels are positively correlated with
126 hase (CBS) deficiency, a genetic disorder in homocysteine (Hcy) metabolism in humans, elevates plasma
127 ded by genes at 5q14 and 21q22.3 function in homocysteine (Hcy) metabolism, and index SNPs for each h
128                          Accumulation of the homocysteine (Hcy) precursor S-adenosylhomocysteine (Ado
129  showed reduced levels of enzymes catalyzing homocysteine (Hcy) production and recycling, together wi
130            Biothiols such as cysteine (Cys), homocysteine (Hcy), and glutathione (GSH) play crucial r
131           Biothiols, such as cysteine (Cys), homocysteine (Hcy), and glutathione (GSH), play a key ro
132    In addition, structures are presented for homocysteine (Hcy), D-Cys, thiosulfate, and azide bound
133 for specific detection of cysteine (Cys) and homocysteine (Hcy).
134                                   Because of homocysteine (HCys) belonging to the thiol and amino gro
135 e conversion of S-methylmethionine (SMM) and homocysteine (HCys) to two equivalents of methionine.
136 eceptors that mediate oscillatory control of homocysteine homeostasis in mice.
137 ession of DNMT1, MMP9, TIMP1, and S-adenosyl homocysteine hydrolase (SAHH) and upregulated methylene
138 logs of the SAH hydrolase Ahcy (S-adenosyl-L-homocysteine hydrolase [SAHH[), CG9977/dAhcyL1 and Ahcy8
139 he accumulation of methylmalonic acid and/or homocysteine in blood and urine.
140  conclude that mild to moderate elevation of homocysteine in Cbs(+/-) mice is accompanied by progress
141                          Severe elevation of homocysteine in cbs(-/-) mutant mice is accompanied by a
142 EG/SEG, supporting a possible causal role of homocysteine in EG/SEG.
143 lodiphosphate (GSPP) along with S-adenosyl-L-homocysteine in the cofactor binding site, resulting fro
144 IKV NS5 protein in complex with S-adenosyl-L-homocysteine, in which the tandem methyltransferase (MTa
145 lalanine, cyanylated cysteine, or cyanylated homocysteine incorporated at different positions within
146 001) in unsupplemented women, whereas plasma homocysteine increased (6.6 +/- 2.3 to 7.6 +/- 2.3 mumol
147 ri cannot utilize the other product of LuxS, homocysteine, indicating that phenotypes of luxS mutants
148                  Diets containing ethanol or homocysteine induced hyperhomocysteinemia and glucose in
149                            Here we show that homocysteine-induced ER protein (Herp), a protein highly
150 ave previously identified a link between the homocysteine-induced suppression of the selenoprotein gl
151  identified known ERAD factors such as Hrd1; homocysteine-inducible, endoplasmic reticulum stress-ind
152  base-promoted intramolecular cyclization of homocysteine into Dha formed a stable cystathionine (thi
153 ents of one-carbon metabolism, remethylating homocysteine into methionine and providing methyl groups
154                  An understanding of whether homocysteine is a cause or a marker of increased blood p
155                              Elevated plasma homocysteine is a risk factor for Alzheimer disease, but
156                                       Excess homocysteine is a risk factor for cardiovascular disease
157                                  High plasma homocysteine is associated with increased risk of CRC, w
158        Folate B12-dependent remethylation of homocysteine is important, but less is understood about
159                                              Homocysteine is metabolized to methionine by the action
160 Met metabolism changes, and increased plasma homocysteine is more apparent.
161 ternatively, by the transulfuration pathway, homocysteine is transformed to hydrogen sulphide (H2S),
162 ystathionine (R-S-(2-amino-2-carboxyethyl)-l-homocysteine) is a non-proteinogenic thioether containin
163 c acid, glutamine, glycine, histidine, total homocysteine, isoleucine, kynurenine, leucine, lysine, m
164 und to be associated with elevated levels of homocysteine, known as hyperhomocysteinemia.
165 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
166  OR = 1.50; 95% CI = 1.01-2.23) and elevated homocysteine levels (>15 micromol/L: OR = 2.24; 95% CI =
167 omisation the association among MTHFR C677T, homocysteine levels and WMH, approached, but did not rea
168 trials focusing on elderly subjets with high homocysteine levels are warranted to see if progression
169                 In the placebo group, higher homocysteine levels at baseline are associated with fast
170 d Relevance: MTHFR polymorphism and elevated homocysteine levels contributed separately and jointly t
171             If these findings are confirmed, homocysteine levels may be a therapeutic target to reduc
172 t out another deleterious trait of disturbed homocysteine levels that could participate in the aetiol
173  possible pathway of MTHFR polymorphisms via homocysteine levels to cortical cataract.
174 lue Mountains Eye Study 2 cohort with normal homocysteine levels was 68.3 (8.1) years and 73.2 (8.5)
175                                        Serum homocysteine levels were assessed following standard met
176 t, the second survey serves as baseline when homocysteine levels were assessed, and 5-year incidence
177        Combined CT/TT genotypes and elevated homocysteine levels were associated with a 3-fold risk o
178                              Increased total homocysteine levels were associated with faster rates of
179 eractions between MTHFR and child folate and homocysteine levels were observed for wheezing and asthm
180 ssociations of MTHFR polymorphisms and serum homocysteine levels with incident cortical cataract in a
181                     Plasma lipid profile and homocysteine levels, blood pressure, oxidative stress, a
182 rials demonstrated that despite reduction in homocysteine levels, disease outcome remained unaffected
183  synthesis and significantly decreased serum homocysteine levels.
184 r blood glucose, serum cholesterol, or serum homocysteine levels.
185 and 73.2 (8.5) years for those with elevated homocysteine levels.
186 cortical cataract was partially mediated via homocysteine levels.
187 PEX included blood glucose, cholesterol, and homocysteine levels; blood pressure; and cardiac morbidi
188 ) polymorphisms have been shown to influence homocysteine levels; homocysteine has been implicated as
189                                              Homocysteine lowering by using B vitamins had no signifi
190  for Alzheimer disease, but the relevance of homocysteine lowering to slow the rate of cognitive agin
191 xaenoic acid) modify the treatment effect of homocysteine-lowering B vitamins on brain atrophy rates
192 sease (CAD) and the null associations in the homocysteine-lowering trials have prompted the need to i
193                                         Most homocysteine-lowering trials with folate and vitamins B6
194 high-sensitivity C-reactive protein <2 mg/L, homocysteine &lt;10 micromol/L, N-terminal pro-brain natriu
195 tors VIII/IX/XI, fibrinogen, lipoprotein(a), homocysteine, lupus anticoagulant, anticardiolipin antib
196                                              Homocysteine may interact with both risk factors and pro
197  timing of expression of genes that regulate homocysteine metabolism and the liver responses to ethan
198  timing in expression of genes that regulate homocysteine metabolism compared with control mice.
199 vel mechanism for H2S-mediated regulation of homocysteine metabolism in cardiomyocytes, and a negativ
200   FA plays an established role in folate and homocysteine metabolism, but the means by which it suppr
201 a novel role in promoting H2S production and homocysteine metabolism, which may have therapeutic valu
202  Folate, choline, and betaine participate in homocysteine metabolism.
203              Here we report the binding of L-homocysteine, methionine, and several folate analogs.
204 in B-12 deficiency increases choline use for homocysteine methylation.
205 betaine (N,N,N-trimethylglycine) via betaine-homocysteine methyltransferase (BHMT), which is expresse
206 ent methylation pathway-catalyzed by betaine-homocysteine methyltransferase (BHMT)-for establishing a
207  also found expression of the enzyme betaine homocysteine methyltransferase in cortical neurons.
208            We studied C57Bl/6J Bhmt (betaine-homocysteine methyltransferase)-null mice at age 4, 12,
209 structures identify interactions between the homocysteine moiety and the 5'-alkylthiol binding site o
210 been described, the interactions between the homocysteine moiety of SAH and the 5'-alkylthiol binding
211  define severe MTHFR deficiency, methionine, homocysteine, MTHFR enzyme activity in fibroblasts, or m
212   Six thiols (mercaptoacetic acid, cysteine, homocysteine, N-acetyl-cysteine, mercaptoethane-sulfonat
213 erhomocysteinemia was defined as total serum homocysteine of 12 micromol/L or greater.
214 erhomocysteinemia was defined as total serum homocysteine of 12 mumol/L or greater.
215                    However, effect of H2S or homocysteine on CBS and CSE expression, and cross-talk b
216 he aim was to assess the causal influence of homocysteine on systolic and diastolic blood pressure (S
217 orrectly oriented for an in-line attack by l-homocysteine on the N(5)-methyl.
218                    We show that binding of L-homocysteine or methionine results in conformational rea
219        Furthermore, each 2-fold increment in homocysteine or methylmalonic acid concentration was ass
220  HL1 cardiomyocytes with increasing doses of homocysteine or Na2S/GYY4137, a H2S donor, and measured
221 sulfur metabolism to cysteine synthesis from homocysteine or utilize cysteine and/or homocysteine for
222 the genetics of 1-carbon pathway metabolism, homocysteine, oxidative stress, endothelial dysfunction,
223 8), treatment with beta-blockers (P = 0.03), homocysteine (P = 0.02), and glutamylcysteine (P = 0.003
224  increased methylmalonic acid (P<0.01-0.04), homocysteine (P<0.01), cystathionine (P<0.01), and the d
225 nthase and gamma-cystathionase (CSE) and for homocysteine persulfide synthesis from homocystine by CS
226 ylation, promoted by the accumulation of the homocysteine precursor SAH, suppresses GPx-1 expression
227 he decreased S-adenosylmethionine/S-adenosyl homocysteine ratio (P<0.01).
228                                   Initially, homocysteine reacts with native catalase and/or redox-ac
229 omplex with aclacinomycin T and S-adenosyl-L-homocysteine refined to 1.9-A resolution revealed that t
230 o thymidylate biosynthesis at the expense of homocysteine remethylation during folate deficiency.
231 ate synthesis occurs in the nucleus, whereas homocysteine remethylation occurs in the cytosol.
232 plementation did not affect in vivo rates of homocysteine remethylation or the appearance of homocyst
233 indicated that the thymidylate synthesis and homocysteine remethylation pathways compete for a limiti
234 holine can be used as a source of methyl for homocysteine remethylation to methionine, but choline sy
235 erved in folate deficiency at the expense of homocysteine remethylation, but the mechanisms are unkno
236                      In vivo fluxes of total homocysteine remethylation, the remethylation of homocys
237 switch from cystathionine to cysteine and/or homocysteine renders H2S synthesis by CSE responsive to
238          We investigated maternal folate and homocysteine responses and related effects in the newbor
239                                Expression of homocysteine-responsive endoplasmic reticulum-resident u
240                                      Betaine-homocysteine S-methyltransferase (BHMT) activity is only
241 eterodimer partner [SHP]-null mice), betaine-homocysteine S-methyltransferase (Bhmt), or both genes (
242 t the design and synthesis of poly(S-alkyl-L-homocysteine)s, which were found to be a new class of re
243 sence of its methyl donor product S-adenosyl-homocysteine (SAH) and its ortholog scTrm10 from Sacchar
244 sibly reflected in high levels of S-adenosyl-homocysteine (SAH) and low levels of S-adenosyl-methioni
245  NTMT1 in complex with cofactor S-adenosyl-L-homocysteine (SAH) and six substrate peptides, respectiv
246 y/mass spectrometry (LC/MS)-based S-adenosyl homocysteine (SAH) detection assay for histone methyltra
247                 The affinity of S-adenosyl-l-homocysteine (SAH) for SAM binding proteins was used to
248      Here, we describe a suite of S-adenosyl homocysteine (SAH) photoreactive probes and their applic
249 tive fluorescent biosensors for S-adenosyl-l-homocysteine (SAH) that provide a direct "mix and go" ac
250 m7)G0pppA1G2U3U4G5U6U7-3'), and S-adenosyl-l-homocysteine (SAH), the by-product of the methylation re
251 h is converted via methylation to S-adenosyl-homocysteine (SAH), which accumulates during aging.
252 cond SAM (SAM2) is converted to S-adenosyl-l-homocysteine (SAH).
253 uman tRNA3(Lys) and the product S-adenosyl-L-homocysteine show a dimer of heterodimers in which each
254 exhibited higher selectivity toward cysteine/homocysteine than toward other amino acids and thiol-con
255 arding the associations between plasma total homocysteine (tHcy) and B vitamin levels and age-related
256 linked hearing loss to elevated plasma total homocysteine (tHcy) and folate deficiency, and have show
257 ecrease of approximately 75% in plasma total homocysteine (tHcy) and normalization of cysteine concen
258 rong observational association between total homocysteine (tHcy) concentrations and risk of coronary
259                   tCys, methionine and total homocysteine (tHcy) increased with age.
260             Moderately elevated plasma total homocysteine (tHcy) is a strong modifiable risk factor f
261                        Elevated total plasma homocysteine (tHcy) is considered to be an independent c
262              In 148 stable RTRs, total serum homocysteine (tHcy) level, folate, serum albumin and cre
263 vious data suggest that elevated serum total homocysteine (tHcy) may be a risk factor for bone fractu
264 ntake is positively related and total plasma homocysteine (tHcy) negatively related to academic succe
265 choline, betaine, dimethylglycine, and total homocysteine (tHcy) were measured longitudinally at <12,
266 s of vitamin B-12, holotranscobalamin, total homocysteine (tHcy), and methylmalonic acid (MMA) were m
267 ancy with the use of plasma cobalamin, total homocysteine (tHcy), and methylmalonic acid (MMA).
268 measurement of serum cobalamin, plasma total homocysteine (tHcy), and plasma methylmalonic acid (MMA)
269 ined by combining vitamin B-12, plasma total homocysteine (tHcy), methylmalonic acid (MMA), and holot
270 c evidence of a relation between serum total homocysteine (tHcy), vitamin B-12, and folate and age-re
271 bolism characterized by elevated serum total homocysteine (tHcy).
272 In 2SLS regression, for the same increase in homocysteine, the coefficients were -1.8 mm Hg for SBP (
273 onine synthase (MS) catalyzes methylation of homocysteine, the last step in the biosynthesis of methi
274 s in body composition.On the basis of plasma homocysteine, the NOAEL of supplemented Met intake is 46
275 -methyl-tetrahydrofolate-glutamate3 to the l-homocysteine thiol.
276 servations for the aminolysis of N-acetyl-dl-homocysteine thiolactone with n-butylamine in THF and CH
277 -methyl-tetrahydrofolate-glutamate3 to the L-homocysteine thiolate to generate methionine.
278 elial cells (HRECs) were treated with excess homocysteine to analyze permeability.
279                     CBS condenses serine and homocysteine to cystathionine with the help of three cof
280 enes into the unprecedented S-oxygenation of homocysteine to engender the corresponding sulfenic acid
281 onine cycle, in which folate and B12 convert homocysteine to methionine, which is in turn converted t
282 itamin B12 functions in the remethylation of homocysteine to methionine, which regenerates THF from 5
283   This enzyme catalyzes the remethylation of homocysteine to methionine, with betaine as the methyl d
284  the four DNA bases and the remethylation of homocysteine to methionine.
285  purine nucleotides and for remethylation of homocysteine to methionine.
286 and result in a hypothesis about the role of homocysteine-to-Cys interconversion and Asn biosynthesis
287                           Conversely, in the homocysteine-treated cardiomyocytes, CBS and miR-133a we
288                                              Homocysteine-treated HRECs showed increased permeability
289                                We found that homocysteine upregulates CSE but downregulates CBS where
290 rs, for instance by lowering elevated plasma homocysteine using B vitamins.
291 tion were assessed via questionnaires.Plasma homocysteine was elevated with the highest dose of suppl
292                         The association with homocysteine was significant for proximal colon tumors (
293 folate, serum vitamin B-12, and plasma total homocysteine were determined.
294 cy because combined abnormalities of MMA and homocysteine were very frequent and the concentrations t
295                                        Serum homocysteine, when studied singly, has been reported to
296  following chain of events: B vitamins lower homocysteine, which directly leads to a decrease in GM a
297 R)-hydroxyproline and proline by cysteine or homocysteine, which reduces the preorganization and ther
298                                     Lowering homocysteine with combined vitamin B-12 and folic acid s
299     The association of genetically increased homocysteine with DBP was not consistent across differen
300 nt enzyme that catalyzes the condensation of homocysteine with serine or with cysteine to form cystat

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