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1 und to H3K36M or H3K36I peptides with SAH (S-adenosylhomocysteine).
2 ession and increasing S-adenosylmethionine/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 with its cofactor S-adenosylmethionine or S-adenosylhomocysteine.
8 S-adenosylmethionine to form sarcosine and S-adenosylhomocysteine.
9 A prior to release of the reaction product S-adenosylhomocysteine.
10 sphate and the methyltransferase inhibitor S-adenosylhomocysteine.
11 nsferase enzymes because of high levels of S-adenosylhomocysteine.
12 ce and presence of S-adenosylmethionine or S-adenosylhomocysteine.
13 RMT10) in complex with a reaction product, S-adenosylhomocysteine.
14 llular hypomethylation from an increase in S-adenosylhomocysteine (5), an inhibitor of methyltransfer
15 sylhomocysteine and adenine by recombinant S-adenosylhomocysteine/5'-methylthioadenosine nucleosidase
16 ysteine to dramatically increase levels of S-adenosylhomocysteine, a potent inhibitor of methyltransf
18 tivity was inhibited by AdoMet metabolites S-adenosylhomocysteine, adenosine, 5'-deoxyadenosine, S-me
19 To examine the interaction of AdoMet and S-adenosylhomocysteine (AdoCys), isothermal titration calo
20 p < 0.01) and a 3-fold increase in hepatic S-adenosylhomocysteine (AdoHcy) (p < 0.01) concentrations,
21 ich catalyzes the reversible hydrolysis of S-adenosylhomocysteine (AdoHcy) has been determined at 2.8
23 (MDL 28,842), an irreversible inhibitor of S-adenosylhomocysteine (AdoHcy) hydrolase (EC 3.3.1.1), ex
26 sparagine 191 (N191) in the active site of S-adenosylhomocysteine (AdoHcy) hydrolase have been mutate
28 ign more specific and potent inhibitors of S-adenosylhomocysteine (AdoHcy) hydrolase, we investigated
31 evels of S-adenosylmethionine (AdoMet) and S-adenosylhomocysteine (AdoHcy) in plasma can be measured
32 lation of the homocysteine (Hcy) precursor S-adenosylhomocysteine (AdoHcy) may cause cellular hypomet
34 H) to hydrolyze the methyltransfer product S-adenosylhomocysteine (AdoHcy) to homocysteine (Hcy) and
35 inhibition studies with methylated DNA and S-adenosylhomocysteine (AdoHcy) were obtained and evaluate
39 o N-methylglycine (sarcosine) and produces S-adenosylhomocysteine (AdoHcy), thereby controlling the m
40 by-product of transmethylation reactions, S-adenosylhomocysteine (AdoHcy), which causes by-product i
48 TL1-WDR4-tRNA with S-adenosylmethionine or S-adenosylhomocysteine along with METTL1 crystal structure
49 show that PoyC catalyzes the formation of S-adenosylhomocysteine and 5'-deoxyadenosine and the trans
50 o produce expected RS methylase coproducts S-adenosylhomocysteine and 5'-deoxyadenosine, and to requi
51 not the prototypical MTAN substrates (e.g. S-adenosylhomocysteine and 5'-methylthioadenosine), is hyd
52 ts for AdoMet with those for the uncharged S-adenosylhomocysteine and 5'-methylthioadenosine, and the
53 erase in a pseudo-bisubstrate complex with S-adenosylhomocysteine and a HEPES ion reveals an all-beta
54 the conversion of S-adenosylmethionine to S-adenosylhomocysteine and can be applied to any methyltra
55 e betaine supplementation failed to reduce S-adenosylhomocysteine and did not positively affect any o
56 gh the enhanced formation of intracellular S-adenosylhomocysteine and disruption of focal adhesion co
57 of the PfPMT-D128A mutant in complex with S-adenosylhomocysteine and either pEA or phosphocholine re
58 nd the other with the protein complexed to S-adenosylhomocysteine and its dTDP-linked sugar product.
60 osylmethionine (SAM) to glycine generating S-adenosylhomocysteine and sarcosine (N-methylglycine).
61 ition studies with the substrate analogues S-adenosylhomocysteine and sinefungin gave competitive inh
64 complex comprising VP39, coenzyme product S-adenosylhomocysteine, and a 5' m7 G-capped, single-stran
65 ill also deaminate 5'-methylthioadenosine, S-adenosylhomocysteine, and adenosine to a small extent.
66 tly increased, while S-adenosylmethionine, S-adenosylhomocysteine, and cystathionine exhibited non-mo
67 plasma levels of homocysteine, methionine, S-adenosylhomocysteine, and S-adenosylmethionine were all
68 These effects were reproduced not only by S-adenosylhomocysteine (another methylation inhibitor), bu
71 SAM itself plays this role, giving rise to S-adenosylhomocysteine as a coproduct of the reaction.
73 t was inhibited by S-adenosylethionine and S-adenosylhomocysteine but not by sinfungin or methionine.
74 nd 52 wk (N = 8) and observed elevation of S-adenosylhomocysteine concentrations and development of p
76 was annotated as a 5'-methylthioadenosine/S-adenosylhomocysteine deaminase (EC 3.5.4.31/3.5.4.28).
77 osidase) and LuxS (terminal synthase) from S-adenosylhomocysteine, directly increased Escherichia col
79 he substrate, initiating hydride shift and S-adenosylhomocysteine elimination to complete the formati
81 ith other amino acids, such as methionine, S-adenosylhomocysteine, homoserine, or homoserine lactone,
84 A site-directed mutagenesis, D244E, of S-adenosylhomocysteine hydrolase (AdoHcyase) changes drast
85 atocyte cell line, HepG2, with inhibitors of adenosylhomocysteine hydrolase (AHCY) known to increase
87 overproduction, activity and expression of S-adenosylhomocysteine hydrolase (converts S-adenosylhomoc
88 tococcus pneumoniae 5'-methylthioadenosine/S-adenosylhomocysteine hydrolase (MTAN) catalyzes the hydr
89 methionine alpha,gamma-lyase (rMETase) and S-adenosylhomocysteine hydrolase (rSAHH) cloned from Pseud
91 n's disease (WD) through the inhibition of S-adenosylhomocysteine hydrolase (SAHH) by copper (Cu) and
92 identical or nearly identical to predicted S-adenosylhomocysteine hydrolase (SAHH) from two Nicotiana
95 d for methylation cycle enzymes, including S-adenosylhomocysteine hydrolase (SAHH), the only known en
96 regulated H19 lncRNA binds to and inhibits S-adenosylhomocysteine hydrolase (SAHH), the only mammalia
97 n a Superose column fraction that contains S-adenosylhomocysteine hydrolase (SAHH), which has a high
98 sed molecular beacon (MB) used for probing S-adenosylhomocysteine hydrolase (SAHH)-catalyzed hydrolys
99 f adenosine, based on adenosine inhibiting S-adenosylhomocysteine hydrolase (SAHH)-catalyzed hydrolys
102 hanistic findings reveal that TMAO targets S-adenosylhomocysteine hydrolase and disrupts the methioni
103 eomics study reveals that two other genes (S-Adenosylhomocysteine hydrolase and Serine hydroxymethylt
104 cells to nucleoside analogue inhibitors of S-adenosylhomocysteine hydrolase correlates directly with
106 es of methionine adenosyltransferase II or S-adenosylhomocysteine hydrolase in the brain tissue of th
107 deoxyadenosine and dATP, and inhibition of S-adenosylhomocysteine hydrolase in the thymus, spleen, an
109 enosine, as well resulting dATP levels and S-adenosylhomocysteine hydrolase inhibition in bone marrow
110 se neither homocysteine thiolactone nor an S-adenosylhomocysteine hydrolase inhibitor (adenosine dial
111 dy, we demonstrate that treatment with the S-adenosylhomocysteine hydrolase inhibitor 3-deazaneplanoc
114 d by expressing the Pseudomonas aeruginosa S-adenosylhomocysteine hydrolase that synthesizes homocyst
115 H19 deficiency increased the activity of S-adenosylhomocysteine hydrolase, a regulator of DNA methy
116 of nine nucleoside analogue inhibitors of S-adenosylhomocysteine hydrolase, an important target for
117 ation, S-adenosylmethionine synthetase and S-adenosylhomocysteine hydrolase, are increased in respons
118 nistically, TMAO noncompetitively inhibits S-adenosylhomocysteine hydrolase, leading to accumulation
119 ion, adenosine dialdehyde, an inhibitor of S-adenosylhomocysteine hydrolase, was found to block cytok
122 nged in an Arabidopsis mutant deficient in S-adenosylhomocysteine hydrolase1 (SAHH1) during early see
123 basis of the available X-ray structures of S-adenosylhomocysteine hydrolases (SAHHs), free energy sim
124 elevation of all forms of homocysteine and S-adenosylhomocysteine in the liver compared to Tg-hCBS Cb
125 th sinefungin, a nonhydrolyzable analog of S-adenosylhomocysteine, increases the rate of deamidated H
126 de, and the competitive product inhibitor, S-adenosylhomocysteine, inhibited such covalent labeling o
127 ng and release of S-adenosylmethionine and S-adenosylhomocysteine is manifested as a hybrid ping-pong
128 referred order of product release in which S-adenosylhomocysteine is released from enzyme before full
129 The structure of PKMT1 in complex with S-adenosylhomocysteine is solved to a resolution of 1.9 A.
130 ted whether the precursor of homocysteine, S-adenosylhomocysteine, is a more sensitive indicator of r
131 ysteine metabolism favors the formation of S-adenosylhomocysteine, leading to inhibition of methyltra
132 te diet is associated with increased brain S-adenosylhomocysteine levels, PPMT downregulation, reduce
134 A synthon approach from the analogues of S-adenosylhomocysteine, methionine, and deoxycytidine reca
135 duced by 74 and 40%, respectively, whereas S-adenosylhomocysteine, methylthioadenosine, and global DN
136 es not inhibit NSP14 activity; and second, S-adenosylhomocysteine modestly activates NSP14 exonucleas
140 e biosynthesis with 5'-methylthioadenosine/S-adenosylhomocysteine nucleosidase (MTAN) catalyzing an e
144 a 26-kDa protein as 5'-methylthioadenosine/S-adenosylhomocysteine nucleosidase (Pfs-2), previously de
146 ia coli mtn gene, a 5'-methylthioadenosine/S-adenosylhomocysteine nucleosidase, which hydrolyses 5'-m
148 a toxic effect of Se-adenosylmethionine, Se-adenosylhomocysteine, or of any compound in the methioni
149 inemia was accompanied by higher levels of S-adenosylhomocysteine (p < 0.05) and lower S-adenosylmeth
151 ociated with a higher S-adenosylmethionine/S-adenosylhomocysteine ratio and lower cystathione beta-sy
152 ation potential (the S-adenosylmethionine: S-adenosylhomocysteine ratio) in the developing brain was
153 , which lead to a low intracellular AdoMet/S-adenosylhomocysteine ratio, are associated with faster e
155 (p < 0.05) and lower S-adenosylmethionine/S-adenosylhomocysteine ratios (p < 0.001) in liver and bra
156 5-Methyltetrahydrofolate, SAM, and SAM/S-adenosylhomocysteine ratios were lower in FASD and Mthfr
158 hat incubation of neuroblastoma cells with S-adenosylhomocysteine results in reduced methylation of p
159 S-adenosylmethionine through intermediates S-adenosylhomocysteine, ribosylhomocysteine, homocysteine,
160 bolite concentrations (total homocysteine, S-adenosylhomocysteine, S-adenosylmethionine, vitamin B(12
162 ecause an increased intracellular ratio of S-adenosylhomocysteine/S-adenosylmethionine favors inhibit
163 and designed a series of N(6)-substituted S-adenosylhomocysteine (SAH) analogues that are targeted t
164 requires the presence of either AdoMet or S-adenosylhomocysteine (SAH) and a strong reducing agent s
165 er has been crystallized with an inhibitor S-adenosylhomocysteine (SAH) and a substrate guanidinoacet
166 e hydrolase (SAHH)-catalyzed hydrolysis of S-adenosylhomocysteine (SAH) and for sensing adenosine bas
167 er hypothalamic S-adenosylmethionine (SAM):S-adenosylhomocysteine (SAH) and global DNA methylation co
168 uding increased levels of homocysteine and S-adenosylhomocysteine (SAH) and reduced levels of S-adeno
169 h homocysteine, is produced by cleavage of S-adenosylhomocysteine (SAH) and S-ribosylhomocysteine by
170 tructural analysis of the RNA complexed to S-adenosylhomocysteine (SAH) and sinefungin and by measuri
171 tion of SAM results in rapid production of S-adenosylhomocysteine (SAH) and the mCys residue, while t
172 y in dtp mutants led to elevated levels of S-adenosylhomocysteine (SAH) and, to a lesser degree, of i
173 d hydrolysis of the methylation by-product S-adenosylhomocysteine (SAH) by S-adenosylhomocysteinase (
176 xidative metabolism genes cytochrome P450, S-adenosylhomocysteine (SAH) hydrolase, cysteine sulfinic
177 s of this RNA motif specifically recognize S-adenosylhomocysteine (SAH) in protein-free in vitro assa
182 udies have revealed that increased adipose S-adenosylhomocysteine (SAH) levels generate methylation d
184 e viperin (residues 45-362) complexed with S-adenosylhomocysteine (SAH) or 5'-deoxyadenosine (5'-dAdo
185 y acted together to decrease the liver SAM/S-adenosylhomocysteine (SAH) ratio and to increase liver S
187 ol diet, the S-adenosylmethionine (SAM) to S-adenosylhomocysteine (SAH) ratio was lower in the liver
189 a was shown to catalyze the deamination of S-adenosylhomocysteine (SAH) to S-inosylhomocysteine (SIH)
190 nents of this pathway because they convert S-adenosylhomocysteine (SAH) to S-ribosylhomocysteine (SRH
191 ns its SAM pool exclusively by methylating S-adenosylhomocysteine (SAH) using a synthetic methyl dono
192 d cell (RBC) folate, vitamin B12, SAM, and S-Adenosylhomocysteine (SAH) were analyzed in cord blood.
193 ase (PCT), S-adenosylmethionine (SAM), and S-adenosylhomocysteine (SAH) were measured in liver homoge
194 the ratio of S-adenosylmethionine (SAM) to S-adenosylhomocysteine (SAH) were significantly reduced in
195 our different adenosine-based metabolites: S-adenosylhomocysteine (SAH), 5'-methylthioadenosine (MTA)
196 by induction of the enzyme that hydrolyzes S-adenosylhomocysteine (SAH), a product and inhibitor of m
197 of methionine, S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), adenosine, homocysteine, cys
198 synthesis, increasing the ratio of SAM to S-adenosylhomocysteine (SAH), and inhibiting the apoptosis
199 enosylmethionine (SAM), elevation in liver S-adenosylhomocysteine (SAH), and reduction in the SAM/SAH
200 ion potential, higher creatinine, betaine, S-adenosylhomocysteine (SAH), and S-adenosylmethionine (SA
201 correlations between gene expression, Hcy, S-adenosylhomocysteine (SAH), and S-adenosylmethionine (SA
202 rat liver GAMT has been crystallized with S-adenosylhomocysteine (SAH), and the crystal structure ha
204 es of wild-type HpMTAN cocrystallized with S-adenosylhomocysteine (SAH), Formycin A (FMA), and (3R,4S
205 osylmethionine (SAM), the reaction product S-adenosylhomocysteine (SAH), or the SAH analog sinefungin
207 M)-dependent methylation reactions produce S-adenosylhomocysteine (SAH), the precursor of homocystein
209 e, methionine, S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), vitamin B-12, and adenosine
210 simultaneously produced via hydrolysis of S-adenosylhomocysteine (SAH), we hypothesized that hHcys m
211 these, including 5-methylthioadenosine and S-adenosylhomocysteine (SAH), were tested as substrates, a
226 d bound to the S-adenosylmethionine analog S-adenosylhomocysteine (SAH, 2.15 A resolution) and the an
227 le intermediates, s-adenosylmethionine and s-adenosylhomocysteine, suggesting that a methylation cycl
228 yme, and the concentration ratio of AdoMet:S-adenosylhomocysteine, the breakdown product of AdoMet an
229 ric enzyme that catalyzes the breakdown of S-adenosylhomocysteine to adenosine and homocysteine and i
230 se (AdoHcyase) catalyzes the hydrolysis of S-adenosylhomocysteine to form adenosine and homocysteine.
232 from methionine to S-adenosylmethionine to S-adenosylhomocysteine to homocysteine, and the removal of
233 substrate S-adenosylmethionine (SAM), with S-adenosylhomocysteine unable to restore the condensation
240 S-adenosylmethionine (major methyl donor):S-adenosylhomocysteine) were reduced in maternal liver.
241 tion that allows greater solvent access to S-adenosylhomocysteine, which is almost completely buried
242 After methylation, SAM is converted to S-adenosylhomocysteine, which is further metabolized to ad
243 d the product of the methylation reaction, S-adenosylhomocysteine, with much higher affinity (KD of 0