ライフサイエンスコーパス: S-adenosylhomocysteine

1 bound to H3K36M or H3K36I peptides with SAH (S-adenosylhomocysteine).

2 pression and increasing S-adenosylmethionine/S-adenosylhomocysteine.

3 n DNA hypomethylation via pathways involving S-adenosylhomocysteine.

4 reduction in the plasma S-adenosylmethionine/S-adenosylhomocysteine.

5 tide bearing Lys-20 and the product cofactor S-adenosylhomocysteine.

6 to stack against the adenine of the cofactor S-adenosylhomocysteine.

7 ex with its cofactor S-adenosylmethionine or S-adenosylhomocysteine.

8 y S-adenosylmethionine to form sarcosine and S-adenosylhomocysteine.

9 DNA prior to release of the reaction product S-adenosylhomocysteine.

10 hosphate and the methyltransferase inhibitor S-adenosylhomocysteine.

11 ransferase enzymes because of high levels of S-adenosylhomocysteine.

12 ence and presence of S-adenosylmethionine or S-adenosylhomocysteine.

13 tPRMT10) in complex with a reaction product, S-adenosylhomocysteine.

14 cellular hypomethylation from an increase in S-adenosylhomocysteine (5), an inhibitor of methyltransf

15 bosylhomocysteine and adenine by recombinant S-adenosylhomocysteine/5'-methylthioadenosine nucleosida

16 ocysteine to dramatically increase levels of S-adenosylhomocysteine, a potent inhibitor of methyltran

17 S-Adenosylhomocysteine acted as a pseudosubstrate, in th

18 activity was inhibited by AdoMet metabolites S-adenosylhomocysteine, adenosine, 5'-deoxyadenosine, S-

19 To examine the interaction of AdoMet and S-adenosylhomocysteine (AdoCys), isothermal titration ca

20 (p < 0.01) and a 3-fold increase in hepatic S-adenosylhomocysteine (AdoHcy) (p < 0.01) concentration

21 which catalyzes the reversible hydrolysis of S-adenosylhomocysteine (AdoHcy) has been determined at 2

22 Human placental S-adenosylhomocysteine (AdoHcy) hydrolase (EC 3.3.1.1) w

23 e (MDL 28,842), an irreversible inhibitor of S-adenosylhomocysteine (AdoHcy) hydrolase (EC 3.3.1.1),

24 S-Adenosylhomocysteine (AdoHcy) hydrolase catalyzes the

25 Most inhibitors of S-adenosylhomocysteine (AdoHcy) hydrolase function as su

26 asparagine 191 (N191) in the active site of S-adenosylhomocysteine (AdoHcy) hydrolase have been muta

27 Comparison of crystal structures of S-adenosylhomocysteine (AdoHcy) hydrolase in the substra

28 esign more specific and potent inhibitors of S-adenosylhomocysteine (AdoHcy) hydrolase, we investigat

29 were tested as inhibitors of human placenta S-adenosylhomocysteine (AdoHcy) hydrolase.

30 were very potent irreversible inhibitors of S-adenosylhomocysteine (AdoHcy) hydrolase.

31 levels of S-adenosylmethionine (AdoMet) and S-adenosylhomocysteine (AdoHcy) in plasma can be measure

32 mulation of the homocysteine (Hcy) precursor S-adenosylhomocysteine (AdoHcy) may cause cellular hypom

33 Accumulation of the S-adenosylhomocysteine (AdoHcy) product, a feedback inhi

34 AHH) to hydrolyze the methyltransfer product S-adenosylhomocysteine (AdoHcy) to homocysteine (Hcy) an

35 t inhibition studies with methylated DNA and S-adenosylhomocysteine (AdoHcy) were obtained and evalua

36 The assay was designed to detect S-adenosylhomocysteine (AdoHcy), a product of all S-aden

37 active cofactor AdoMet, its reaction product S-adenosylhomocysteine (AdoHcy), and adenosine.

38 S-Adenosylhomocysteine (AdoHcy), formed after donation o

39 to N-methylglycine (sarcosine) and produces S-adenosylhomocysteine (AdoHcy), thereby controlling the

40 he by-product of transmethylation reactions, S-adenosylhomocysteine (AdoHcy), which causes by-product

41 precursor of homocysteine in all tissues is S-adenosylhomocysteine (AdoHcy).

42 nity of Ecm1 for sinefungin versus AdoMet or S-adenosylhomocysteine (AdoHcy).

43 ethyl donor S-adenosylmethionine (AdoMet) to S-adenosylhomocysteine (AdoHcy).

44 ity in AdoMet binding and weak inhibition by S-adenosylhomocysteine (AdoHcy).

45 levels of S-adenosylmethionine (AdoMet) and S-adenosylhomocysteine (AdoHcy).

46 s strongly inhibited by the reaction product S-adenosylhomocysteine (AdoHcy).

47 S-Adenosylhomocysteine-agarose selected enzymes that uti

48 ETTL1-WDR4-tRNA with S-adenosylmethionine or S-adenosylhomocysteine along with METTL1 crystal structu

49 We show that PoyC catalyzes the formation of S-adenosylhomocysteine and 5'-deoxyadenosine and the tra

50 to produce expected RS methylase coproducts S-adenosylhomocysteine and 5'-deoxyadenosine, and to req

51 t not the prototypical MTAN substrates (e.g. S-adenosylhomocysteine and 5'-methylthioadenosine), is h

52 ults for AdoMet with those for the uncharged S-adenosylhomocysteine and 5'-methylthioadenosine, and t

53 sferase in a pseudo-bisubstrate complex with S-adenosylhomocysteine and a HEPES ion reveals an all-be

54 rs the conversion of S-adenosylmethionine to S-adenosylhomocysteine and can be applied to any methylt

55 ose betaine supplementation failed to reduce S-adenosylhomocysteine and did not positively affect any

56 ough the enhanced formation of intracellular S-adenosylhomocysteine and disruption of focal adhesion

57 es of the PfPMT-D128A mutant in complex with S-adenosylhomocysteine and either pEA or phosphocholine

58 and the other with the protein complexed to S-adenosylhomocysteine and its dTDP-linked sugar product

59 Following methyl group transfer, S-adenosylhomocysteine and monomethylated polypeptide di

60 enosylmethionine (SAM) to glycine generating S-adenosylhomocysteine and sarcosine (N-methylglycine).

61 ibition studies with the substrate analogues S-adenosylhomocysteine and sinefungin gave competitive i

62 The structure of a complex with S-adenosylhomocysteine and two molecules of tetrahydropa

63 talyze the deamination of guanine, cytosine, S-adenosylhomocysteine, and 8-oxoguanine.

64 ry complex comprising VP39, coenzyme product S-adenosylhomocysteine, and a 5' m7 G-capped, single-str

65 will also deaminate 5'-methylthioadenosine, S-adenosylhomocysteine, and adenosine to a small extent.

66 ently increased, while S-adenosylmethionine, S-adenosylhomocysteine, and cystathionine exhibited non-

67 t plasma levels of homocysteine, methionine, S-adenosylhomocysteine, and S-adenosylmethionine were al

68 These effects were reproduced not only by S-adenosylhomocysteine (another methylation inhibitor),

69 Plasma S-adenosylhomocysteine appears to be a much more sensiti

70 Both plasma total homocysteine and S-adenosylhomocysteine are significantly correlated with

71 , SAM itself plays this role, giving rise to S-adenosylhomocysteine as a coproduct of the reaction.

72 t), sinefungin (inhibitor), and both pEA and S-adenosylhomocysteine bound were determined.

73 ort was inhibited by S-adenosylethionine and S-adenosylhomocysteine but not by sinfungin or methionin

74 and 52 wk (N = 8) and observed elevation of S-adenosylhomocysteine concentrations and development of

75 Methionine, S-adenosylmethionine, S-adenosylhomocysteine, cysteine, choline, betaine, and

76 at was annotated as a 5'-methylthioadenosine/S-adenosylhomocysteine deaminase (EC 3.5.4.31/3.5.4.28).

77 leosidase) and LuxS (terminal synthase) from S-adenosylhomocysteine, directly increased Escherichia c

78 h SAM (dmin = 2.3 A) or the reaction product S-adenosylhomocysteine (dmin = 1.6 A).

79 the substrate, initiating hydride shift and S-adenosylhomocysteine elimination to complete the forma

80 Accumulation of homocysteine and S-adenosylhomocysteine, genome-wide DNA hypomethylation,

81 with other amino acids, such as methionine, S-adenosylhomocysteine, homoserine, or homoserine lacton

82 S-Adenosylhomocysteine hydrolase (AdoHcy hydrolase) crys

83 S-Adenosylhomocysteine hydrolase (AdoHcyase) catalyzes t

84 A site-directed mutagenesis, D244E, of S-adenosylhomocysteine hydrolase (AdoHcyase) changes dra

85 ed a causative mutation in the gene encoding S-adenosylhomocysteine hydrolase (Ahcy).

86 y overproduction, activity and expression of S-adenosylhomocysteine hydrolase (converts S-adenosylhom

87 eptococcus pneumoniae 5'-methylthioadenosine/S-adenosylhomocysteine hydrolase (MTAN) catalyzes the hy

88 s methionine alpha,gamma-lyase (rMETase) and S-adenosylhomocysteine hydrolase (rSAHH) cloned from Pse

89 S-adenosylhomocysteine hydrolase (SAH) is a key enzyme i

90 son's disease (WD) through the inhibition of S-adenosylhomocysteine hydrolase (SAHH) by copper (Cu) a

91 r identical or nearly identical to predicted S-adenosylhomocysteine hydrolase (SAHH) from two Nicotia

92 S-Adenosylhomocysteine hydrolase (SAHH) is an NAD(+)-dep

93 This assay utilizes S-adenosylhomocysteine hydrolase (SAHH) to hydrolyze the

94 hed for methylation cycle enzymes, including S-adenosylhomocysteine hydrolase (SAHH), the only known

95 y regulated H19 lncRNA binds to and inhibits S-adenosylhomocysteine hydrolase (SAHH), the only mammal

96 in a Superose column fraction that contains S-adenosylhomocysteine hydrolase (SAHH), which has a hig

97 based molecular beacon (MB) used for probing S-adenosylhomocysteine hydrolase (SAHH)-catalyzed hydrol

98 of adenosine, based on adenosine inhibiting S-adenosylhomocysteine hydrolase (SAHH)-catalyzed hydrol

99 T1A), glycine-N-methyltransferase (GNMT) and S-adenosylhomocysteine hydrolase (SAHH).

100 NA methylation by modulating the activity of S-adenosylhomocysteine hydrolase (SAHH).

101 echanistic findings reveal that TMAO targets S-adenosylhomocysteine hydrolase and disrupts the methio

102 oteomics study reveals that two other genes (S-Adenosylhomocysteine hydrolase and Serine hydroxymethy

103 L cells to nucleoside analogue inhibitors of S-adenosylhomocysteine hydrolase correlates directly wit

104 uding accumulation of dATP and inhibition of S-adenosylhomocysteine hydrolase enzyme activity.

105 ties of methionine adenosyltransferase II or S-adenosylhomocysteine hydrolase in the brain tissue of

106 f deoxyadenosine and dATP, and inhibition of S-adenosylhomocysteine hydrolase in the thymus, spleen,

107 hymus and spleen, and a marked inhibition of S-adenosylhomocysteine hydrolase in these organs.

108 adenosine, as well resulting dATP levels and S-adenosylhomocysteine hydrolase inhibition in bone marr

109 ause neither homocysteine thiolactone nor an S-adenosylhomocysteine hydrolase inhibitor (adenosine di

110 tudy, we demonstrate that treatment with the S-adenosylhomocysteine hydrolase inhibitor 3-deazaneplan

111 ibited following treatment with a reversible S-adenosylhomocysteine hydrolase inhibitor, DZ2002.

112 S-Adenosylhomocysteine hydrolase is not involved because

113 red by expressing the Pseudomonas aeruginosa S-adenosylhomocysteine hydrolase that synthesizes homocy

114 H19 deficiency increased the activity of S-adenosylhomocysteine hydrolase, a regulator of DNA met

115 es of nine nucleoside analogue inhibitors of S-adenosylhomocysteine hydrolase, an important target fo

116 ylation, S-adenosylmethionine synthetase and S-adenosylhomocysteine hydrolase, are increased in respo

117 hanistically, TMAO noncompetitively inhibits S-adenosylhomocysteine hydrolase, leading to accumulatio

118 ction, adenosine dialdehyde, an inhibitor of S-adenosylhomocysteine hydrolase, was found to block cyt

119 Furthermore, introduction of S-adenosylhomocysteine hydrolase, which restores the met

120 by complementation with a gene encoding the S-adenosylhomocysteine hydrolase.

121 hanged in an Arabidopsis mutant deficient in S-adenosylhomocysteine hydrolase1 (SAHH1) during early s

122 e basis of the available X-ray structures of S-adenosylhomocysteine hydrolases (SAHHs), free energy s

123 d elevation of all forms of homocysteine and S-adenosylhomocysteine in the liver compared to Tg-hCBS

124 with sinefungin, a nonhydrolyzable analog of S-adenosylhomocysteine, increases the rate of deamidated

125 fide, and the competitive product inhibitor, S-adenosylhomocysteine, inhibited such covalent labeling

126 ding and release of S-adenosylmethionine and S-adenosylhomocysteine is manifested as a hybrid ping-po

127 preferred order of product release in which S-adenosylhomocysteine is released from enzyme before fu

128 The structure of PKMT1 in complex with S-adenosylhomocysteine is solved to a resolution of 1.9

129 gated whether the precursor of homocysteine, S-adenosylhomocysteine, is a more sensitive indicator of

130 ocysteine metabolism favors the formation of S-adenosylhomocysteine, leading to inhibition of methylt

131 late diet is associated with increased brain S-adenosylhomocysteine levels, PPMT downregulation, redu

132 s of glutathione and S-adenosylmethionine to S-adenosylhomocysteine levels, respectively.

133 A synthon approach from the analogues of S-adenosylhomocysteine, methionine, and deoxycytidine re

134 reduced by 74 and 40%, respectively, whereas S-adenosylhomocysteine, methylthioadenosine, and global

135 does not inhibit NSP14 activity; and second, S-adenosylhomocysteine modestly activates NSP14 exonucle

136 The importance of methylthioadenosine/S-adenosylhomocysteine (MTA/SAH) nucleosidase in bacteri

137 Methylthioadenosine/S-adenosylhomocysteine nucleosidase (MTAN) catalyzes rea

138 5'-Methylthioadenosine/S-adenosylhomocysteine nucleosidase (MTAN) catalyzes the

139 one biosynthesis with 5'-methylthioadenosine/S-adenosylhomocysteine nucleosidase (MTAN) catalyzing an

140 The bacterial 5'-methylthioadenosine/S-adenosylhomocysteine nucleosidase (MTAN) enzyme is a m

141 Bacterial 5'-methylthioadenosine/ S-adenosylhomocysteine nucleosidase (MTAN) hydrolyzes ad

142 tate of S. pneumoniae 5'-methylthioadenosine/S-adenosylhomocysteine nucleosidase (MTAN).

143 d a 26-kDa protein as 5'-methylthioadenosine/S-adenosylhomocysteine nucleosidase (Pfs-2), previously

144 chia coli mtn gene, a 5'-methylthioadenosine/S-adenosylhomocysteine nucleosidase, which hydrolyses 5'

145 Also, S-adenosylhomocysteine or methyl donor deficiency inhibi

146 teinemia was accompanied by higher levels of S-adenosylhomocysteine (p < 0.05) and lower S-adenosylme

147 A decreased S-adenosylmethionine: S-adenosylhomocysteine ratio and increased methionine we

148 ssociated with a higher S-adenosylmethionine/S-adenosylhomocysteine ratio and lower cystathione beta-

149 ylation potential (the S-adenosylmethionine: S-adenosylhomocysteine ratio) in the developing brain wa

150 um, which lead to a low intracellular AdoMet/S-adenosylhomocysteine ratio, are associated with faster

151 thylation and hence the S-adenosylmethionine/S-adenosylhomocysteine ratio.

152 ne (p < 0.05) and lower S-adenosylmethionine/S-adenosylhomocysteine ratios (p < 0.001) in liver and b

153 5-Methyltetrahydrofolate, SAM, and SAM/S-adenosylhomocysteine ratios were lower in FASD and Mth

154 18 and 4.6 +/- 0.5 microM for sinefungin and S-adenosylhomocysteine, respectively.

155 that incubation of neuroblastoma cells with S-adenosylhomocysteine results in reduced methylation of

156 m S-adenosylmethionine through intermediates S-adenosylhomocysteine, ribosylhomocysteine, homocystein

157 tabolite concentrations (total homocysteine, S-adenosylhomocysteine, S-adenosylmethionine, vitamin B(

158 S-Adenosylmethionine, S-adenosylhomocysteine, S-ribosylhomocysteine, homocyste

159 Because an increased intracellular ratio of S-adenosylhomocysteine/S-adenosylmethionine favors inhib

160 ch and designed a series of N(6)-substituted S-adenosylhomocysteine (SAH) analogues that are targeted

161 1+ requires the presence of either AdoMet or S-adenosylhomocysteine (SAH) and a strong reducing agent

162 iver has been crystallized with an inhibitor S-adenosylhomocysteine (SAH) and a substrate guanidinoac

163 ine hydrolase (SAHH)-catalyzed hydrolysis of S-adenosylhomocysteine (SAH) and for sensing adenosine b

164 ower hypothalamic S-adenosylmethionine (SAM):S-adenosylhomocysteine (SAH) and global DNA methylation

165 cluding increased levels of homocysteine and S-adenosylhomocysteine (SAH) and reduced levels of S-ade

166 ith homocysteine, is produced by cleavage of S-adenosylhomocysteine (SAH) and S-ribosylhomocysteine b

167 structural analysis of the RNA complexed to S-adenosylhomocysteine (SAH) and sinefungin and by measu

168 dition of SAM results in rapid production of S-adenosylhomocysteine (SAH) and the mCys residue, while

169 ity in dtp mutants led to elevated levels of S-adenosylhomocysteine (SAH) and, to a lesser degree, of

170 pid hydrolysis of the methylation by-product S-adenosylhomocysteine (SAH) by S-adenosylhomocysteinase

171 S(MK) box RNA; in contrast, the addition of S-adenosylhomocysteine (SAH) had no effect.

172 rough increasing the association of ADK with S-adenosylhomocysteine (SAH) hydrolase (SAHH).

173 oxidative metabolism genes cytochrome P450, S-adenosylhomocysteine (SAH) hydrolase, cysteine sulfini

174 les of this RNA motif specifically recognize S-adenosylhomocysteine (SAH) in protein-free in vitro as

175 as with bound S-adenosylmethionine (SAM) or S-adenosylhomocysteine (SAH) in the catalytic site.

176 S-adenosylhomocysteine (SAH) is a negative regulator of

177 S-adenosylhomocysteine (SAH) is product of methionine in

178 Notably, maternal and progeny plasma S-adenosylhomocysteine (SAH) levels are both elevated af

179 studies have revealed that increased adipose S-adenosylhomocysteine (SAH) levels generate methylation

180 ment with SAMe doubled intracellular MTA and S-adenosylhomocysteine (SAH) levels.

181 use viperin (residues 45-362) complexed with S-adenosylhomocysteine (SAH) or 5'-deoxyadenosine (5'-dA

182 ncy acted together to decrease the liver SAM/S-adenosylhomocysteine (SAH) ratio and to increase liver

183 SAM level and SAM:S-adenosylhomocysteine (SAH) ratio increased by 50-75% a

184 trol diet, the S-adenosylmethionine (SAM) to S-adenosylhomocysteine (SAH) ratio was lower in the live

185 The SAM level, SAM-to-S-adenosylhomocysteine (SAH) ratio, and DNA methylation

186 ima was shown to catalyze the deamination of S-adenosylhomocysteine (SAH) to S-inosylhomocysteine (SI

187 ponents of this pathway because they convert S-adenosylhomocysteine (SAH) to S-ribosylhomocysteine (S

188 ains its SAM pool exclusively by methylating S-adenosylhomocysteine (SAH) using a synthetic methyl do

189 ood cell (RBC) folate, vitamin B12, SAM, and S-Adenosylhomocysteine (SAH) were analyzed in cord blood

190 erase (PCT), S-adenosylmethionine (SAM), and S-adenosylhomocysteine (SAH) were measured in liver homo

191 d the ratio of S-adenosylmethionine (SAM) to S-adenosylhomocysteine (SAH) were significantly reduced

192 four different adenosine-based metabolites: S-adenosylhomocysteine (SAH), 5'-methylthioadenosine (MT

193 d by induction of the enzyme that hydrolyzes S-adenosylhomocysteine (SAH), a product and inhibitor of

194 s of methionine, S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), adenosine, homocysteine, c

195 10 synthesis, increasing the ratio of SAM to S-adenosylhomocysteine (SAH), and inhibiting the apoptos

196 adenosylmethionine (SAM), elevation in liver S-adenosylhomocysteine (SAH), and reduction in the SAM/S

197 ation potential, higher creatinine, betaine, S-adenosylhomocysteine (SAH), and S-adenosylmethionine (

198 d correlations between gene expression, Hcy, S-adenosylhomocysteine (SAH), and S-adenosylmethionine (

199 nt rat liver GAMT has been crystallized with S-adenosylhomocysteine (SAH), and the crystal structure

200 S-Adenosylmethionine and S-adenosylhomocysteine (SAH), as the substrate and produ

201 ures of wild-type HpMTAN cocrystallized with S-adenosylhomocysteine (SAH), Formycin A (FMA), and (3R,

202 enosylmethionine (SAM), the reaction product S-adenosylhomocysteine (SAH), or the SAH analog sinefung

203 Blood biomarkers of these nutrients, S-adenosylhomocysteine (SAH), S-adenosylmethionine (SAM)

204 SAM)-dependent methylation reactions produce S-adenosylhomocysteine (SAH), the precursor of homocyste

205 S-adenosylhomocysteine (SAH), the product formed when th

206 ine, methionine, S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), vitamin B-12, and adenosin

207 re simultaneously produced via hydrolysis of S-adenosylhomocysteine (SAH), we hypothesized that hHcys

208 f these, including 5-methylthioadenosine and S-adenosylhomocysteine (SAH), were tested as substrates,

209 SARS-CoV-2 NSP14 by forming a unique ternary S-adenosylhomocysteine (SAH)-bound complex.

210 C-glycosylation reminiscent of NAD-dependent S-adenosylhomocysteine (SAH)-hydrolase catalysis.

211 -adenosylmethionine (SAM) and its metabolite S-adenosylhomocysteine (SAH).

212 rocedure specifically detects and quantifies S-adenosylhomocysteine (SAH).

213 hibition by SFG than by the reaction product S-adenosylhomocysteine (SAH).

214 nto the mitochondrial matrix in exchange for S-adenosylhomocysteine (SAH).

215 only mammalian enzyme capable of hydrolysing S-adenosylhomocysteine (SAH).

216 as a negative regulator that responds to the S-adenosylhomocysteine (SAH).

217 pper (Cu) and the consequent accumulation of S-adenosylhomocysteine (SAH).

218 ine hydrolase (SAHH)-catalyzed hydrolysis of S-adenosylhomocysteine (SAH).

219 S-adenosylmethionine (SAM) and inhibited by S-adenosylhomocysteine (SAH).

220 AM), and increasing the demethylated product S-adenosylhomocysteine (SAH).

221 on inhibitors, methylthioadenosine (MTA) and S-adenosylhomocysteine (SAH).

222 duced ratio of s-adenosylmethionine (SAM) to s-adenosylhomocysteine (SAH).

223 and bound to the S-adenosylmethionine analog S-adenosylhomocysteine (SAH, 2.15 A resolution) and the

224 ycle intermediates, s-adenosylmethionine and s-adenosylhomocysteine, suggesting that a methylation cy

225 nzyme, and the concentration ratio of AdoMet:S-adenosylhomocysteine, the breakdown product of AdoMet

226 meric enzyme that catalyzes the breakdown of S-adenosylhomocysteine to adenosine and homocysteine and

227 lase (AdoHcyase) catalyzes the hydrolysis of S-adenosylhomocysteine to form adenosine and homocystein

228 f S-adenosylhomocysteine hydrolase (converts S-adenosylhomocysteine to Hcy) were both increased.

229 , from methionine to S-adenosylmethionine to S-adenosylhomocysteine to homocysteine, and the removal

230 cosubstrate S-adenosylmethionine (SAM), with S-adenosylhomocysteine unable to restore the condensatio

231 The structure of RumA/RNA/S-adenosylhomocysteine uncovers the mechanism for achiev

232 The S-adenosylhomocysteine values were 40.0 +/- 20.6 (32.3,

233 The K m for S-adenosylhomocysteine was approximately 15-fold higher

234 Lastly, S-adenosylhomocysteine was approximately twice normal an

235 Product inhibition by S-adenosylhomocysteine was competitive versus S-adenosyl

236 , 5'-methylthioadenosine, cystathionine, and S-adenosylhomocysteine were downregulated.

237 of S-adenosylmethionine (major methyl donor):S-adenosylhomocysteine) were reduced in maternal liver.

238 mation that allows greater solvent access to S-adenosylhomocysteine, which is almost completely burie

239 After methylation, SAM is converted to S-adenosylhomocysteine, which is further metabolized to

240 ind the product of the methylation reaction, S-adenosylhomocysteine, with much higher affinity (KD of