ライフサイエンスコーパス: adenosylhomocysteine

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

2 with its cofactor S-adenosylmethionine or S-adenosylhomocysteine.

3 DNA hypomethylation via pathways involving S-adenosylhomocysteine.

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

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

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

7 S-adenosylmethionine to form sarcosine and S-adenosylhomocysteine.

8 A prior to release of the reaction product S-adenosylhomocysteine.

9 nsferase enzymes because of high levels of S-adenosylhomocysteine.

10 ce and presence of S-adenosylmethionine or S-adenosylhomocysteine.

11 RMT10) in complex with a reaction product, S-adenosylhomocysteine.

12 ession and increasing S-adenosylmethionine/S-adenosylhomocysteine.

13 llular hypomethylation from an increase in S-adenosylhomocysteine (5), an inhibitor of methyltransfer

14 sylhomocysteine and adenine by recombinant S-adenosylhomocysteine/5'-methylthioadenosine nucleosidase

15 ysteine to dramatically increase levels of S-adenosylhomocysteine, a potent inhibitor of methyltransf

16 S-Adenosylhomocysteine acted as a pseudosubstrate, in that

17 tivity was inhibited by AdoMet metabolites S-adenosylhomocysteine, adenosine, 5'-deoxyadenosine, S-me

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

19 p < 0.01) and a 3-fold increase in hepatic S-adenosylhomocysteine (AdoHcy) (p < 0.01) concentrations,

20 ich catalyzes the reversible hydrolysis of S-adenosylhomocysteine (AdoHcy) has been determined at 2.8

21 Human placental S-adenosylhomocysteine (AdoHcy) hydrolase (EC 3.3.1.1) was

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

23 S-Adenosylhomocysteine (AdoHcy) hydrolase catalyzes the re

24 Most inhibitors of S-adenosylhomocysteine (AdoHcy) hydrolase function as subs

25 sparagine 191 (N191) in the active site of S-adenosylhomocysteine (AdoHcy) hydrolase have been mutate

26 Comparison of crystal structures of S-adenosylhomocysteine (AdoHcy) hydrolase in the substrate

27 ign more specific and potent inhibitors of S-adenosylhomocysteine (AdoHcy) hydrolase, we investigated

28 ere tested as inhibitors of human placenta S-adenosylhomocysteine (AdoHcy) hydrolase.

29 ere very potent irreversible inhibitors of S-adenosylhomocysteine (AdoHcy) hydrolase.

30 evels of S-adenosylmethionine (AdoMet) and S-adenosylhomocysteine (AdoHcy) in plasma can be measured

31 lation of the homocysteine (Hcy) precursor S-adenosylhomocysteine (AdoHcy) may cause cellular hypomet

32 Accumulation of the S-adenosylhomocysteine (AdoHcy) product, a feedback inhibi

33 H) to hydrolyze the methyltransfer product S-adenosylhomocysteine (AdoHcy) to homocysteine (Hcy) and

34 inhibition studies with methylated DNA and S-adenosylhomocysteine (AdoHcy) were obtained and evaluate

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

36 tive cofactor AdoMet, its reaction product S-adenosylhomocysteine (AdoHcy), and adenosine.

37 S-Adenosylhomocysteine (AdoHcy), formed after donation of

38 o N-methylglycine (sarcosine) and produces S-adenosylhomocysteine (AdoHcy), thereby controlling the m

39 by-product of transmethylation reactions, S-adenosylhomocysteine (AdoHcy), which causes by-product i

40 recursor of homocysteine in all tissues is S-adenosylhomocysteine (AdoHcy).

41 ty of Ecm1 for sinefungin versus AdoMet or S-adenosylhomocysteine (AdoHcy).

42 hyl donor S-adenosylmethionine (AdoMet) to S-adenosylhomocysteine (AdoHcy).

43 y in AdoMet binding and weak inhibition by S-adenosylhomocysteine (AdoHcy).

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

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

46 S-Adenosylhomocysteine-agarose selected enzymes that utili

47 show that PoyC catalyzes the formation of S-adenosylhomocysteine and 5'-deoxyadenosine and the trans

48 o produce expected RS methylase coproducts S-adenosylhomocysteine and 5'-deoxyadenosine, and to requi

49 not the prototypical MTAN substrates (e.g. S-adenosylhomocysteine and 5'-methylthioadenosine), is hyd

50 ts for AdoMet with those for the uncharged S-adenosylhomocysteine and 5'-methylthioadenosine, and the

51 erase in a pseudo-bisubstrate complex with S-adenosylhomocysteine and a HEPES ion reveals an all-beta

52 the conversion of S-adenosylmethionine to S-adenosylhomocysteine and can be applied to any methyltra

53 e betaine supplementation failed to reduce S-adenosylhomocysteine and did not positively affect any o

54 gh the enhanced formation of intracellular S-adenosylhomocysteine and disruption of focal adhesion co

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

56 nd the other with the protein complexed to S-adenosylhomocysteine and its dTDP-linked sugar product.

57 Following methyl group transfer, S-adenosylhomocysteine and monomethylated polypeptide diss

58 osylmethionine (SAM) to glycine generating S-adenosylhomocysteine and sarcosine (N-methylglycine).

59 ition studies with the substrate analogues S-adenosylhomocysteine and sinefungin gave competitive inh

60 The structure of a complex with S-adenosylhomocysteine and two molecules of tetrahydropapa

61 lyze the deamination of guanine, cytosine, S-adenosylhomocysteine, and 8-oxoguanine.

62 complex comprising VP39, coenzyme product S-adenosylhomocysteine, and a 5' m7 G-capped, single-stran

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

64 plasma levels of homocysteine, methionine, S-adenosylhomocysteine, and S-adenosylmethionine were all

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

66 Plasma S-adenosylhomocysteine appears to be a much more sensitive

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

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

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

70 t was inhibited by S-adenosylethionine and S-adenosylhomocysteine but not by sinfungin or methionine.

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

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

73 osidase) and LuxS (terminal synthase) from S-adenosylhomocysteine, directly increased Escherichia col

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

75 he substrate, initiating hydride shift and S-adenosylhomocysteine elimination to complete the formati

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

77 ith other amino acids, such as methionine, S-adenosylhomocysteine, homoserine, or homoserine lactone,

78 S-Adenosylhomocysteine hydrolase (AdoHcy hydrolase) crysta

79 S-Adenosylhomocysteine hydrolase (AdoHcyase) catalyzes the

80 A site-directed mutagenesis, D244E, of S-adenosylhomocysteine hydrolase (AdoHcyase) changes drast

81 atocyte cell line, HepG2, with inhibitors of adenosylhomocysteine hydrolase (AHCY) known to increase

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

83 overproduction, activity and expression of S-adenosylhomocysteine hydrolase (converts S-adenosylhomoc

84 tococcus pneumoniae 5'-methylthioadenosine/S-adenosylhomocysteine hydrolase (MTAN) catalyzes the hydr

85 methionine alpha,gamma-lyase (rMETase) and S-adenosylhomocysteine hydrolase (rSAHH) cloned from Pseud

86 S-adenosylhomocysteine hydrolase (SAH) is a key enzyme in

87 n's disease (WD) through the inhibition of S-adenosylhomocysteine hydrolase (SAHH) by copper (Cu) and

88 identical or nearly identical to predicted S-adenosylhomocysteine hydrolase (SAHH) from two Nicotiana

89 S-Adenosylhomocysteine hydrolase (SAHH) is an NAD(+)-depen

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

91 d for methylation cycle enzymes, including S-adenosylhomocysteine hydrolase (SAHH), the only known en

92 regulated H19 lncRNA binds to and inhibits S-adenosylhomocysteine hydrolase (SAHH), the only mammalia

93 n a Superose column fraction that contains S-adenosylhomocysteine hydrolase (SAHH), which has a high

94 sed molecular beacon (MB) used for probing S-adenosylhomocysteine hydrolase (SAHH)-catalyzed hydrolys

95 f adenosine, based on adenosine inhibiting S-adenosylhomocysteine hydrolase (SAHH)-catalyzed hydrolys

96 A), glycine-N-methyltransferase (GNMT) and S-adenosylhomocysteine hydrolase (SAHH).

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

98 eomics study reveals that two other genes (S-Adenosylhomocysteine hydrolase and Serine hydroxymethylt

99 cells to nucleoside analogue inhibitors of S-adenosylhomocysteine hydrolase correlates directly with

100 ing accumulation of dATP and inhibition of S-adenosylhomocysteine hydrolase enzyme activity.

101 es of methionine adenosyltransferase II or S-adenosylhomocysteine hydrolase in the brain tissue of th

102 deoxyadenosine and dATP, and inhibition of S-adenosylhomocysteine hydrolase in the thymus, spleen, an

103 mus and spleen, and a marked inhibition of S-adenosylhomocysteine hydrolase in these organs.

104 enosine, as well resulting dATP levels and S-adenosylhomocysteine hydrolase inhibition in bone marrow

105 se neither homocysteine thiolactone nor an S-adenosylhomocysteine hydrolase inhibitor (adenosine dial

106 dy, we demonstrate that treatment with the S-adenosylhomocysteine hydrolase inhibitor 3-deazaneplanoc

107 ited following treatment with a reversible S-adenosylhomocysteine hydrolase inhibitor, DZ2002.

108 S-Adenosylhomocysteine hydrolase is not involved because n

109 d by expressing the Pseudomonas aeruginosa S-adenosylhomocysteine hydrolase that synthesizes homocyst

110 of nine nucleoside analogue inhibitors of S-adenosylhomocysteine hydrolase, an important target for

111 ation, S-adenosylmethionine synthetase and S-adenosylhomocysteine hydrolase, are increased in respons

112 ion, adenosine dialdehyde, an inhibitor of S-adenosylhomocysteine hydrolase, was found to block cytok

113 Furthermore, introduction of S-adenosylhomocysteine hydrolase, which restores the metab

114 y complementation with a gene encoding the S-adenosylhomocysteine hydrolase.

115 nged in an Arabidopsis mutant deficient in S-adenosylhomocysteine hydrolase1 (SAHH1) during early see

116 basis of the available X-ray structures of S-adenosylhomocysteine hydrolases (SAHHs), free energy sim

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

118 th sinefungin, a nonhydrolyzable analog of S-adenosylhomocysteine, increases the rate of deamidated H

119 de, and the competitive product inhibitor, S-adenosylhomocysteine, inhibited such covalent labeling o

120 ng and release of S-adenosylmethionine and S-adenosylhomocysteine is manifested as a hybrid ping-pong

121 referred order of product release in which S-adenosylhomocysteine is released from enzyme before full

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

123 ted whether the precursor of homocysteine, S-adenosylhomocysteine, is a more sensitive indicator of r

124 ysteine metabolism favors the formation of S-adenosylhomocysteine, leading to inhibition of methyltra

125 te diet is associated with increased brain S-adenosylhomocysteine levels, PPMT downregulation, reduce

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

127 duced by 74 and 40%, respectively, whereas S-adenosylhomocysteine, methylthioadenosine, and global DN

128 The importance of methylthioadenosine/S-adenosylhomocysteine (MTA/SAH) nucleosidase in bacteria

129 Methylthioadenosine/S-adenosylhomocysteine nucleosidase (MTAN) catalyzes react

130 5'-Methylthioadenosine/S-adenosylhomocysteine nucleosidase (MTAN) catalyzes the h

131 e biosynthesis with 5'-methylthioadenosine/S-adenosylhomocysteine nucleosidase (MTAN) catalyzing an e

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

133 te of S. pneumoniae 5'-methylthioadenosine/S-adenosylhomocysteine nucleosidase (MTAN).

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

135 A 5'-methylthioadenosine-adenosylhomocysteine nucleosidase is used to hydrolyze A

136 ia coli mtn gene, a 5'-methylthioadenosine/S-adenosylhomocysteine nucleosidase, which hydrolyses 5'-m

137 Also, S-adenosylhomocysteine or methyl donor deficiency inhibits

138 a toxic effect of Se-adenosylmethionine, Se-adenosylhomocysteine, or of any compound in the methioni

139 inemia was accompanied by higher levels of S-adenosylhomocysteine (p < 0.05) and lower S-adenosylmeth

140 ociated with a higher S-adenosylmethionine/S-adenosylhomocysteine ratio and lower cystathione beta-sy

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

142 ylation and hence the S-adenosylmethionine/S-adenosylhomocysteine ratio.

143 (p < 0.05) and lower S-adenosylmethionine/S-adenosylhomocysteine ratios (p < 0.001) in liver and bra

144 5-Methyltetrahydrofolate, SAM, and SAM/S-adenosylhomocysteine ratios were lower in FASD and Mthfr

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

146 hat incubation of neuroblastoma cells with S-adenosylhomocysteine results in reduced methylation of p

147 S-adenosylmethionine through intermediates S-adenosylhomocysteine, ribosylhomocysteine, homocysteine,

148 S-Adenosylmethionine, S-adenosylhomocysteine, S-ribosylhomocysteine, homocystein

149 ecause an increased intracellular ratio of S-adenosylhomocysteine/S-adenosylmethionine favors inhibit

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

151 requires the presence of either AdoMet or S-adenosylhomocysteine (SAH) and a strong reducing agent s

152 er has been crystallized with an inhibitor S-adenosylhomocysteine (SAH) and a substrate guanidinoacet

153 e hydrolase (SAHH)-catalyzed hydrolysis of S-adenosylhomocysteine (SAH) and for sensing adenosine bas

154 uding increased levels of homocysteine and S-adenosylhomocysteine (SAH) and reduced levels of S-adeno

155 h homocysteine, is produced by cleavage of S-adenosylhomocysteine (SAH) and S-ribosylhomocysteine by

156 tructural analysis of the RNA complexed to S-adenosylhomocysteine (SAH) and sinefungin and by measuri

157 tion of SAM results in rapid production of S-adenosylhomocysteine (SAH) and the mCys residue, while t

158 y in dtp mutants led to elevated levels of S-adenosylhomocysteine (SAH) and, to a lesser degree, of i

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

160 ugh increasing the association of ADK with S-adenosylhomocysteine (SAH) hydrolase (SAHH).

161 xidative metabolism genes cytochrome P450, S-adenosylhomocysteine (SAH) hydrolase, cysteine sulfinic

162 s of this RNA motif specifically recognize S-adenosylhomocysteine (SAH) in protein-free in vitro assa

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

164 S-adenosylhomocysteine (SAH) is a negative regulator of mo

165 S-adenosylhomocysteine (SAH) is product of methionine in t

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

167 nt with SAMe doubled intracellular MTA and S-adenosylhomocysteine (SAH) levels.

168 e viperin (residues 45-362) complexed with S-adenosylhomocysteine (SAH) or 5'-deoxyadenosine (5'-dAdo

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

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

171 ol diet, the S-adenosylmethionine (SAM) to S-adenosylhomocysteine (SAH) ratio was lower in the liver

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

173 a was shown to catalyze the deamination of S-adenosylhomocysteine (SAH) to S-inosylhomocysteine (SIH)

174 nents of this pathway because they convert S-adenosylhomocysteine (SAH) to S-ribosylhomocysteine (SRH

175 ase (PCT), S-adenosylmethionine (SAM), and S-adenosylhomocysteine (SAH) were measured in liver homoge

176 the ratio of S-adenosylmethionine (SAM) to S-adenosylhomocysteine (SAH) were significantly reduced in

177 our different adenosine-based metabolites: S-adenosylhomocysteine (SAH), 5'-methylthioadenosine (MTA)

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

179 of methionine, S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), adenosine, homocysteine, cys

180 synthesis, increasing the ratio of SAM to S-adenosylhomocysteine (SAH), and inhibiting the apoptosis

181 enosylmethionine (SAM), elevation in liver S-adenosylhomocysteine (SAH), and reduction in the SAM/SAH

182 ion potential, higher creatinine, betaine, S-adenosylhomocysteine (SAH), and S-adenosylmethionine (SA

183 correlations between gene expression, Hcy, S-adenosylhomocysteine (SAH), and S-adenosylmethionine (SA

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

185 S-Adenosylmethionine and S-adenosylhomocysteine (SAH), as the substrate and product

186 es of wild-type HpMTAN cocrystallized with S-adenosylhomocysteine (SAH), Formycin A (FMA), and (3R,4S

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

188 M)-dependent methylation reactions produce S-adenosylhomocysteine (SAH), the precursor of homocystein

189 S-adenosylhomocysteine (SAH), the product formed when the

190 e, methionine, S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), vitamin B-12, and adenosine

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

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

193 denosylmethionine (SAM) and its metabolite S-adenosylhomocysteine (SAH).

194 cedure specifically detects and quantifies S-adenosylhomocysteine (SAH).

195 ly mammalian enzyme capable of hydrolysing S-adenosylhomocysteine (SAH).

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

197 er (Cu) and the consequent accumulation of S-adenosylhomocysteine (SAH).

198 e hydrolase (SAHH)-catalyzed hydrolysis of S-adenosylhomocysteine (SAH).

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

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

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

202 ced ratio of s-adenosylmethionine (SAM) to s-adenosylhomocysteine (SAH).

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

204 le intermediates, s-adenosylmethionine and s-adenosylhomocysteine, suggesting that a methylation cycl

205 yme, and the concentration ratio of AdoMet:S-adenosylhomocysteine, the breakdown product of AdoMet an

206 ric enzyme that catalyzes the breakdown of S-adenosylhomocysteine to adenosine and homocysteine and i

207 se (AdoHcyase) catalyzes the hydrolysis of S-adenosylhomocysteine to form adenosine and homocysteine.

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

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

210 substrate S-adenosylmethionine (SAM), with S-adenosylhomocysteine unable to restore the condensation

211 The structure of RumA/RNA/S-adenosylhomocysteine uncovers the mechanism for achievin

212 The S-adenosylhomocysteine values were 40.0 +/- 20.6 (32.3, 47

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

214 Lastly, S-adenosylhomocysteine was approximately twice normal and

215 Product inhibition by S-adenosylhomocysteine was competitive versus S-adenosylme

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

217 tion that allows greater solvent access to S-adenosylhomocysteine, which is almost completely buried

218 d the product of the methylation reaction, S-adenosylhomocysteine, with much higher affinity (KD of 0