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 n DNA hypomethylation via pathways involving S-adenosylhomocysteine.

3 ex with its cofactor S-adenosylmethionine or 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 y S-adenosylmethionine to form sarcosine and S-adenosylhomocysteine.

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

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

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

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

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

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

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

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

16 S-Adenosylhomocysteine acted as a pseudosubstrate, in th

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

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

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

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

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

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

23 S-Adenosylhomocysteine (AdoHcy) hydrolase catalyzes the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 S-Adenosylhomocysteine-agarose selected enzymes that uti

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

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

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

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

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

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

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

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

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

56 and 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 di

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 S-Adenosylhomocysteine hydrolase (AdoHcy hydrolase) crys

79 S-Adenosylhomocysteine hydrolase (AdoHcyase) catalyzes t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 S-Adenosylhomocysteine hydrolase is not involved because

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

129 5'-Methylthioadenosine/S-adenosylhomocysteine nucleosidase (MTAN) catalyzes the

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

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

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

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

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

135 Also, S-adenosylhomocysteine or methyl donor deficiency inhibi

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

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

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

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

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

141 5-Methyltetrahydrofolate, SAM, and SAM/S-adenosylhomocysteine ratios were lower in FASD and Mth

142 18 and 4.6 +/- 0.5 microM for sinefungin and S-adenosylhomocysteine, respectively.

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

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

145 S-Adenosylmethionine, S-adenosylhomocysteine, S-ribosylhomocysteine, homocyste

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

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

148 1+ requires the presence of either AdoMet or S-adenosylhomocysteine (SAH) and a strong reducing agent

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

177 10 synthesis, increasing the ratio of SAM to S-adenosylhomocysteine (SAH), and inhibiting the apoptos

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 Lastly, S-adenosylhomocysteine was approximately twice normal an

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

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

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

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