ライフサイエンスコーパス: Ado

1 Ado alone had little effect upon cell growth.

2 Ado and Ino were simultaneously quantified in homogenize

3 Ado-5'-carboxaldehyde oxime had potent cytotoxicity in t

4 Ado-Cbl and Me-Cbl were susceptible to photolysis, but C

5 Ado-PNP had an apparent K(m) (K(m) ( app)) of 98 +/- 6 m

6 Ado-trastuzumab emtansine (T-DM1) is an antibody-drug co

7 d with both the generated Cbl(II) and .CH(2)-Ado indicating that NO could effectively compete with th

8 oth AdoCbl intermediates (Cbl(II) and .CH(2)-Ado) generated during the enzymatic reaction.

9 I)) and/or the deoxyadenosyl radical (.CH(2)-Ado), both of which are generated from the co-factor of

10 t study, the preclinical efficacy of 8-NH(2)-Ado and its resulting effects on Akt/mTOR and extracellu

11 For all MCL cell lines, 8-NH(2)-Ado inhibited growth and promoted cell death as shown by

12 We conclude that 8-NH(2)-Ado is efficacious in preclinical models of MCL and inhi

13 but maintained their viability with 8-NH(2)-Ado treatment, primary lymphoma cells accumulated higher

14 The efficacy of 8-NH(2)-Ado was highly associated with intracellular accumulatio

15 pamycin (mTOR), we hypothesized that 8-NH(2)-Ado would be active in mantle cell lymphoma (MCL), a hem

16 8-Aminoadenosine (8-NH(2)-Ado), a ribosyl nucleoside analog, in preclinical models

17 Recently, a new class of A(2A) Ado receptor agonists was synthesized.

18 from substrate to form 5'-deoxyadenosine (5'-Ado) and the alpha-Lys* radical (state 3 (Lys*)).

19 s*)), which then abstracts an H-atom from 5'-Ado to form beta-lysine and the 5'-deoxyadenosyl radical

20 Ado R) agonist, selectively activates the A1 Ado R and prolongs atrioventricular (AV) nodal conductio

21 doses lower than those required to cause A2 Ado R-mediated coronary and peripheral vasodilation.

22 hibitor erythro-9(2-hydroxy-3-nonyl)adenine, Ado kinase inhibitor 5'-aminoadenosine, and nucleotide p

23 Adenosine (Ado) and dipyridamole are alternatives to exercise stres

24 Adenosine (Ado) triggers numerous protective mechanisms in the hear

25 Adenosine (Ado) was preferred as a substrate at least 30-fold (Km =

26 Adenosine (Ado)-5'-carboxaldehyde and its 4'-epimer are potent inhi

27 he endogenous antiepileptic agent adenosine (Ado) from the extracellular CNS space.

28 o- < 3'-di- < 3'-triphosphate and adenosine (Ado) < 2'-d-Ado < 2',5'-dd-Ado derivatives, with 2',5'-d

29 Because Hcys and adenosine (Ado) are simultaneously produced via hydrolysis of S-ade

30 rences, namely, dopamine (DA) and adenosine (Ado).

31 AdoHcy) to homocysteine (Hcy) and adenosine (Ado).

32 Monitoring molecules such as adenosine (Ado) and inosine (Ino) in the central nervous system has

33 on was purified and identified as adenosine (Ado).

34 Extracellular ATP, adenosine (Ado), and adenosine plus homocysteine (Ado/HC) cause apo

35 h concentrations of extracellular adenosine (Ado) and deoxyadenosine (dAdo).

36 These effects of extracellular adenosine (Ado) are likely to be mediated by A2a receptor-mediated

37 gement by degrading extracellular adenosine (Ado) to inosine.

38 ol intracellular and interstitial adenosine (Ado) concentrations.

39 nophosphate (AMP) and 2) AMP into adenosine (Ado) via two representative nucleotidases, CD39 and CD73

40 f extracellular and intracellular adenosine (Ado) under hypoxic conditions or in the absence of adeno

41 AH, 5'-methylthioadenosine (MTA), adenosine (Ado), and 5'-deoxyadenosine (5'-dAdo).

42 ause micromolar concentrations of adenosine (Ado) have been documented recently in the interstitial f

43 catalyzes the phosphorylation of adenosine (Ado) to adenosine monophosphate (AMP).

44 Intravenous administration of adenosine (Ado) to patients can cause dyspnoea, chest discomfort an

45 urines and cannot account for the adenosine (Ado) cleavage activity that has been detected in M. tube

46 catalysis of AdoHcy hydrolysis to adenosine (Ado) and homocysteine (Hcy) by means of a redox partial

47 eversible hydrolysis of AdoHcy to adenosine (Ado) and homocysteine (Hcy), playing an essential role i

48 eversible conversion of AdoHcy to adenosine (Ado) and homocysteine (Hcy).

49 ribe a mechanistic model by which adenosine (Ado) signaling results in significant accumulation of SU

50 ng surface metabolism through P1 (adenosine; Ado) receptors.

51 Adenosylcobalamin (Ado-B12) is both the cofactor and inducer of ethanolamin

52 d for the biosynthesis of adenosylcobalamin (Ado-B12).

53 ion occurs in response to adenosylcobalamin (Ado-Cbl) and operates primarily at the translational lev

54 aquocobalamin [H2O-Cbl], adenosylcobalamin [Ado-Cbl], and methylcobalamin [MeCbl]), only the H2O-Cbl

55 rting the dephosphorylation of ATP into Ado, Ado deamination into inosine (Ino), and nucleoside uptak

56 4 +/- 2.6 impulses (P < 0.01, n = 107) after Ado.

57 displays high-affinity binding to ATP, AMP, Ado, AP4A, and alpha,beta Met ADP; however, RPAI-1 does

58 ed by 1,3-dipropyl-8-cyclopentylxanthine, an Ado A1 receptor antagonist, but was unaffected by 3,7-di

59 ence detection (CE-LIF) method that analyzes Ado and Ino by derivatization with 2,4,6-trinitrobenzene

60 The model captures major aspects of ATP and Ado regulation, including their >4-fold increase in conc

61 e achieved with the BDD electrode for DA and Ado was from low nanomolar to high millimolar levels.

62 timal potentials for the detection of DA and Ado were determined to be +740 and +1200 mV versus a pal

63 ic voltammograms were constructed for DA and Ado, and the optimal potentials for the detection of DA

64 The conformational features of H-Lys-Arg-Ado-Ser-Pro-Phe-OH (Ado = 12-aminododecanoic acid), a de

65 ion of dietary cobalamins into coenzyme B12 (Ado-B12), the required cofactor for MCM.

66 f wild-type or dominant active H-Ras blocked Ado/HC-induced apoptosis.

67 e in the Km and an increase in Vmax for both Ado and methyl-Ado.

68 from 6.7+/-0.4 to 14.7+/-0.5 micromol/L, but Ado decreased from 141.7+/-15.1 to 52.4+/-6.8 nmol/L in

69 d a dose-dependent deneddylation of Cul-1 by Ado receptor stimulation predominantly mediated by the A

70 l Ado receptor agonist NECA and abolished by Ado receptor antagonists.

71 ession of ICMT inhibited apoptosis caused by Ado/HC, UV light exposure, or tumor necrosis factor-alph

72 The stimulation of C fibres by Ado was significantly attenuated by pretreatment with am

73 ibosome binding to btuB RNA was inhibited by Ado-Cbl but not by cyanocobalamin, with half-maximal inh

74 res by capsaicin, the C fibre stimulation by Ado had a latency of 6.5 +/- 0.3 s (range, 3-18 s) and l

75 of these new compounds on recombinant canine Ado receptors and to evaluate their hemodynamic properti

76 In assays of recombinant canine Ado receptors, ATL-193 and ATL-146e were highly selectiv

77 PRMT2 contains a highly conserved catalytic Ado-Met binding domain, but the enzymatic function of PR

78 comes through stabilization of the Co(2+)Cbl/Ado. post-homolysis products.

79 8-Cl-Ado activity is dependent on adenosine kinase and requir

80 strate that the cytotoxic metabolite of 8-Cl-Ado and 8-Cl-cAMP is 8-Cl-ATP.

81 on both the exogenous concentration of 8-Cl-Ado and incubation time.

82 e sensitive to the cytotoxic actions of 8-Cl-Ado as caspase-3 activation and the induction of poly-AD

83 requires intracellular accumulation of 8-Cl-Ado as mono-, di-, and tri-phosphates.

84 ffects intracellular purine metabolism; 8-Cl-Ado conversion to succinyl analogs ties its metabolism t

85 To determine MET's role in 8-Cl-Ado cytotoxicity, we generated MM.1S clones stably expre

86 r more RNA polymerases may be mediating 8-Cl-Ado cytotoxicity.

87 hat leukemic lymphocytes incubated with 8-Cl-Ado display time- and dose-dependent increase in the acc

88 Although degradation of 8-Cl-cAMP to 8-Cl-Ado in culture medium or plasma has been shown, cellular

89 serves as a prodrug and is converted to 8-Cl-Ado in medium with subsequent phosphorylation to accumul

90 dissecting the RNA-directed actions of 8-Cl-Ado in MM cells.

91 o model the biochemical consequences of 8-Cl-Ado incorporation into RNA primers, a synthetic RNA prim

92 Both 8-Cl-cAMP and 8-Cl-Ado incubation resulted in the accumulation of 8-Cl-Ado

93 In conclusion, 8-Cl-Ado induces apoptosis in CLL lymphocytes by targeting ce

94 eport a new major metabolic pathway for 8-Cl-Ado intracellular metabolism, the formation of succinyl-

95 Because 8-Cl-Ado is able to overcome survival signals present in MM c

96 our data demonstrate that in MM cells, 8-Cl-Ado is preferentially incorporated into mRNA, suggesting

97 We conclude that 8-Cl-Ado metabolism not only affects intracellular purine met

98 ubation resulted in the accumulation of 8-Cl-Ado mono-, di-, and tri-phosphate (8-Cl-ATP), however, t

99 The cells were incubated with either 8-Cl-Ado or 8-Cl-cAMP to follow the cellular metabolism of th

100 id not accumulate 8-Cl-ATP, either from 8-Cl-Ado or 8-Cl-cAMP, and were resistant to these agents.

101 8-Cl-Ado overcomes MM cell survival by a mechanism that invol

102 Parallel to RNA synthesis inhibition, 8-Cl-Ado was maximally incorporated in the mRNA (>13 nmol/mg

103 on these actions, we hypothesized that 8-Cl-Ado would be ideal to target CLL lymphocytes.

104 ation of succinyl-8-chloro-adenosine (S-8-Cl-Ado) and its monophosphate (S-8-Cl-AMP).

105 8-Chloroadenosine (8-Cl-Ado) is a ribosyl nucleoside analog currently in phase I

106 emonstrated that halogenated adenosine (8-Cl-Ado) was phosphorylated to triphosphate (8-Cl-adenosine

107 he purine analogue, 8-chloro-adenosine (8-Cl-Ado), induces apoptosis in a number of multiple myeloma

108 ucleoside analogue, 8-chloro-adenosine (8-Cl-Ado), is cytotoxic to a number of MM cell lines.

109 r its conversion to 8-chloro-adenosine (8-Cl-Ado).

110 At the 10 microM level of 8-Cl-Ado, >400 microM 8-Cl-ATP accumulated in multiple myelom

111 ription-PCR, and immunoblot analysis on 8-Cl-Ado-treated MM.1S cells and found that the mRNA and prot

112 NA after a 20-h exposure with 10 microM 8-Cl-Ado.

113 xtracellular conversion of 8-Cl-cAMP to 8-Cl-Ado.

114 e secondary metabolites, 8-Cl-ATP and S-8-Cl-Ado.

115 second, novel PNP (Ado-PNP) that can cleave Ado, inosine, and guanosine.

116 ay requires the cofactor adenosyl cobalamin (Ado-B12).

117 In conclusion, Ado stimulates pulmonary C fibre terminals through an ac

118 A solution containing Ado deaminase inhibitor erythro-9(2-hydroxy-3-nonyl)aden

119 Since human cells do not readily convert Ado to Ade, an understanding of the substrate preference

120 acid (ACC) synthase, an enzyme that converts Ado-Met to ACC in ethylene biosynthesis, but not by disr

121 redominantly expressed subtype of Gs-coupled Ado receptors in T cells.

122 < 3'-triphosphate and adenosine (Ado) < 2'-d-Ado < 2',5'-dd-Ado derivatives, with 2',5'-dideoxy-3'ATP

123 ic (larger number of clusters) compared to D-Ado.

124 zyme complexed with 3'-keto-adenosine (D244E.Ado*), we have identified the important amino acid resid

125 The crystal structures of the WT and D244E.Ado*, containing four subunits in the crystallographic a

126 e-refined crystal structures of WT and D244E.Ado*.

127 5'-phosphoryl derivatives of beta-l-2',3'-dd-Ado, and protected phosphoryl derivatives of two 9-(2-ph

128 te and adenosine (Ado) < 2'-d-Ado < 2',5'-dd-Ado derivatives, with 2',5'-dideoxy-3'ATP exhibiting an

129 ivatives of 2',5'-dideoxyadenosine (2',5'-dd-Ado) and beta-l-2',5'-dd-Ado, protected 5'-phosphoryl de

130 adenosine (2',5'-dd-Ado) and beta-l-2',5'-dd-Ado, protected 5'-phosphoryl derivatives of beta-l-2',3'

131 Best studied of these was 2',5'-dd-Ado-3'-O-bis(S-pivaloyl-2-thioethyl)-phosphate, which bl

132 A striking selectivity for 2',5'-dd-Ado-3'-phosphoryl derivatives was observed.

133 inhibited the ability of ecto-ADA to degrade Ado and increased the cAMP response.

134 This review examines deoxyadenosylcobalamin (Ado-B12) biosynthesis, transport, use, and uneven distri

135 efugee complexes of Dadaab, Kenya, and Dollo-Ado, Ethiopia, experienced measles outbreaks during June

136 In Dollo-Ado, 407 cases and 23 deaths (CFR, 5.7%) were reported.

137 rs causes a sustained increase in endogenous Ado production and exerts a potent protective effect aga

138 ish whether sustained increase in endogenous Ado production by the combined application of Ado metabo

139 tabolized to 1,N(6)-ethenoadenosine (epsilon-Ado) as the end product by folliculated oocytes.

140 , show a drastically reduced rate of epsilon-Ado production, epsilon-AMP being the main end-product o

141 nst depletion of the free Met pool by excess Ado-Met synthesis or to regulate Ado-Met level and hence

142 coccus sp. PCC 7002 (S7002) by co-expressing Ado/Aar and Ols and by entirely replacing Ols with three

143 /R cycle-dependent increase in extracellular Ado correlating with increases in the cytoplasmic pool o

144 on of Adk results in increased extracellular Ado, activation of inhibitory Ado A1 receptors, and decr

145 PC and lost in animals lacking extracellular Ado (Cd73-/- mice).

146 as been postulated to regulate extracellular Ado levels, and also the function of CD26 as a co-stimul

147 aling" mechanism, we show that extracellular Ado (extAdo) suppresses all tested T cell receptor (TCR)

148 exes with the inhibitor 2-fluoroadenosine (F-Ado) bound and with the adenosine 5'-(beta,gamma-methyle

149 The binding mode of F-Ado was characterized to illustrate the role of addition

150 ctor ratios (A(H)/A(D)) of 0.16 +/- 0.07 for Ado(*) and 0.5 +/- 0.4 for 8-MeOAdo(*) are observed, bot

151 constants were determined as 4600 M(-1) for Ado and 1000 M(-1) for Ino by CE-LIF.

152 ) - E(H)]) of 3.0 +/- 0.3 kcal mol(-)(1) for Ado(*) and 2.1 +/- 0.6 kcal mol(-)(1) for 8-MeOAdo(*) ha

153 es C: KIE = 12.4 +/- 1.1 at 80 degrees C for Ado(*) and KIE = 12.5 +/- 0.9 at 80 degrees C for 8-MeOA

154 xic moiety in congenital ADA deficiency) for Ado, did not lead to equivalent toxicity.

155 ted in the limit of detection of 1.6 muM for Ado and 4 muM for Ino.

156 mented an ATR-deficient bacterial mutant for Ado-B12-dependent growth on 1,2-propanediol.

157 The longest time constant observed for Ado is approximately 2 ps, and we propose that solute-so

158 nd when ATP, ADP, or AMP was substituted for Ado.

159 ne, which non-selectively activates all four Ado R subtypes and produces unwanted effects, tecadenoso

160 participate in the elimination of water from Ado through the interaction with the 5'-OH group of Ado.

161 Furthermore, Ado/Aar and the non-cyanobacterial enzymes UndA and fatt

162 alpha/SUMO in cells treated with the general Ado receptor agonist NECA and abolished by Ado receptor

163 pression is signaled by internally generated Ado-B12, which can be formed either by the CobA adenosyl

164 s of galactose-induced recombinant yeast had Ado-Met-specific NMTase activities that were highly spec

165 Arabidopsis mutant had significantly higher Ado-Met and lower S-adenosylhomo-Cys levels than the wil

166 sine (Ado), and adenosine plus homocysteine (Ado/HC) cause apoptosis of cultured pulmonary artery end

167 To examine how Ado-Cbl affects translation, the binding of E. coli 30S

168 The homolytic cleavage of the Co(III)-Ado or Co(III)-Me bond resulted in the reduction of the

169 rectifying potassium channels) channels (IK,Ado).

170 In an effort to study the role of AK in Ado homeostasis in the central nervous system, two isofo

171 gation of TCR-triggered growth inhibition in Ado-exposed T cells.

172 onary C fibres may play an important role in Ado-induced adverse respiratory effects.

173 a number of Ado deaminase (ADA) inhibitors, Ado led to significant growth inhibition of all cell lin

174 extracellular Ado, activation of inhibitory Ado A1 receptors, and decreased seizure generation, the

175 supporting the dephosphorylation of ATP into Ado, Ado deamination into inosine (Ino), and nucleoside

176 al step in the conversion of cobalamins into Ado-B12.

177 gand on the electronic properties of Cbls is Ado-cobinamide (AdoCbi(+)), an AdoCbl derivative that la

178 re it binds and methylates STAT3 through its Ado-Met binding domain.

179 to-4',5'-dehydroadenosine to produce 3'-keto-Ado.

180 Cells lacking Ado kinase did not accumulate 8-Cl-ATP, either from 8-Cl

181 ure of Mtb ADK unliganded as well as ligand (Ado) bound at 1.5- and 1.9-A resolution, respectively.

182 ethyl-Met (SMM) from Met and S-adenosyl-Met (Ado-Met).

183 of a trifunctional S-adenosyl L-methionine (Ado-Met): beta-Ala N-methyltransferase (NMTase).

184 an increase in Vmax for both Ado and methyl-Ado.

185 Ks exhibited different affinities for methyl-Ado, with Km values of 79 and 960 microM, respectively,

186 e adenosine analog 2-methyladenosine (methyl-Ado), the first step in the metabolism of this compound

187 Without PMA, adenosine alone (MI+Ado) did not affect the latency to develop I(KATP) (12.3

188 nutes (n=8;P < .02 versus MI, PMA+MI, and MI+Ado groups).

189 d to MI in the presence of adenosine (PMA+MI+Ado), the latency was greatly shortened to 5.5 +/- 1.6 m

190 th half-maximal inhibition around 0.3 microM Ado-Cbl.

191 induced, the EutT transferase supplies more Ado-B12 during the period of high demand.

192 ntraperitoneal injection of the nonselective Ado antagonist theophylline.

193 ed by pyrimidines or caffeine, a nonspecific Ado receptor blocker.

194 at HPC induces extracellular accumulation of Ado and suppresses NF-kappaB activity through deneddylat

195 racellular route that requires the action of Ado kinase.

196 The administration of Ado metabolism inhibitors with nucleotide precursors cau

197 hanism similar to the acetylenic analogue of Ado described previously by Parry et al.

198 do production by the combined application of Ado metabolism inhibitors and nucleotide precursors atte

199 ts known to contribute to the association of Ado to ADA.

200 ion is controlled by the specific binding of Ado-Cbl to btuB RNA, which then affects access to its ri

201 otifs known to be involved in the binding of Ado-Met.

202 fluorescent trinitrophenylated complexes of Ado (TNP-Ado) and Ino (TNP-Ino).

203 xamined the effects of low concentrations of Ado on the growth of cultured human carcinoma cells.

204 lohexyl-5'-N-ethylcarboxamido derivatives of Ado.

205 ft-ventricular injection of the same dose of Ado.

206 oking these adverse reactions, the effect of Ado on single pulmonary C fibres was studied in anaesthe

207 f A2a receptor, CSC, inhibits the effects of Ado and CGS21680; and (4) the increases in [cAMP]i mimic

208 ough the interaction with the 5'-OH group of Ado.

209 enzymes could lead to the identification of Ado analogs that could be selectively activated to toxic

210 ic growth on ethanolamine requires import of Ado-B12 or a precursor (CN-B12 or OH-B12) that can be ad

211 nase activity and feed-forward inhibition of Ado production by ATP and ADP.

212 Right-atrial injection of Ado (320 microg kg-1) activated 68 % (73/107) of pulmona

213 The excited state lifetimes of Ado, Guo, Cyd, and Thd were determined to be 290, 460, 7

214 against the intracellular lymphotoxicity of Ado (and in support of the signaling model) is provided

215 ed by direct intracellular lymphotoxicity of Ado metabolites.

216 Inosine, the metabolite of Ado, did not activate any of eleven C fibres tested in s

217 In the presence of one of a number of Ado deaminase (ADA) inhibitors, Ado led to significant g

218 Finally, the presence of Ado-Cbl elicited formation of a single primer extension-

219 AdoHcy at the beginning and 3'-reduction of Ado at the end of the catalytic cycle) spanning an elimi

220 This hHcys-induced reduction of Ado was also observed in the kidney dialysate.

221 t the SMM cycle contributes to regulation of Ado-Met levels rather than preventing depletion of free

222 regulatory mechanism for a limited supply of Ado-B12.

223 De novo synthesis of Ado-B12 by Salmonella enterica occurs only under anaerob

224 ynamic responses were compared with those of Ado.

225 al features of H-Lys-Arg-Ado-Ser-Pro-Phe-OH (Ado = 12-aminododecanoic acid), a des-Arg(9) analogue of

226 te molecules were detected in experiments on Ado and Cyd by hot ground state absorption at ultraviole

227 phates inhibitory potency followed the order Ado < 2'-dAdo < 2',5'-ddAdo and 3'-mono- < 3'-di- < 3'-t

228 (Aar) and aldehyde deformylating oxygenase (Ado) or olefin synthase (Ols).

229 In rats with chronic hHcys, plasma Ado levels were also significantly decreased.

230 and guanosine only and a second, novel PNP (Ado-PNP) that can cleave Ado, inosine, and guanosine.

231 al structure of Fhit bound to Ado-p-CH2-p-ps-Ado (IB2), a nonhydrolyzable ApppA analog, was refined t

232 Purpose Ado-trastuzumab emtansine (T-DM1) is currently approved

233 ol-d(4) solvent by 5'-deoxyadenosyl radical (Ado(*)) and (ii.) the same H(*) abstraction reactions by

234 noson (CVT-510), a novel adenosine receptor (Ado R) agonist, selectively activates the A1 Ado R and p

235 l by excess Ado-Met synthesis or to regulate Ado-Met level and hence the Ado-Met to S-adenosylhomo-Cy

236 )) and A(H)/A(D) data for a closely related, Ado(*)-mediated H(*) abstraction reaction from a primary

237 of the enzyme activities, decrease in renal Ado levels in hHcys was shown to be associated with inhi

238 ne-5'-0-(2-thiodiphosphate) trilithium salt, Ado-5'-PP[S] stimulation, and limited the ability to mai

239 ne-5'-0-(2-thiodiphosphate) trilithium salt, Ado-5'-PP[S], negated the protection from thrombosis, co

240 The second Ado cleavage activity was identified as 5'-methylthioade

241 and ATL-146e are highly potent and selective Ado A(2A) receptor agonists with excellent potential for

242 reatment with aminophylline, a non-selective Ado receptor antagonist, was completely prevented by 1,3

243 20, rats were treated IT with the selective Ado A1 receptor agonist cyclohexyladenosine (CHA) or veh

244 CobA produces sufficient Ado-B12 to initiate eut operon induction and to serve as

245 sm-based inhibitors, DEA is an acyclic sugar Ado analogue, and the C2' and C3' have opposite chiralit

246 Unlike cyclic sugar Ado analogue inhibitors, including mechanism-based inhib

247 nnected to the protein than the cyclic sugar Ado analogues.

248 res of AdoHcyase complexed with cyclic sugar Ado analogues.

249 drogen bonds as observed in the cyclic sugar Ado complexes.

250 osite chirality to those of the cyclic sugar Ado inhibitors.

251 in the presence of oxygen but can synthesize Ado-B12 only anaerobically.

252 We find that Ado/Aar and Ols can co-exist and that slower growth occu

253 ibition of methylation, we hypothesized that Ado/HC might act by inhibition of isoprenylcysteine-O-ca

254 ing is not modified by EDTA, indicating that Ado structure but not phosphate groups or Ca(2+) is nece

255 The Ado(*) and 8-MeOAdo(*) radicals are generated by Co-C th

256 The Ado/CF combination inhibited DNA synthesis and brought a

257 or stimulation predominantly mediated by the Ado A2B receptor subtype.

258 ter excretion, which could be blocked by the Ado receptor antagonist 8-SPT.

259 s or to regulate Ado-Met level and hence the Ado-Met to S-adenosylhomo-Cys ratio (the methylation rat

260 onfiguration of the N-glycosidic bond in the Ado ligand is inverted [(alpha-ribo)AdoCbl], has been sy

261 expected quantum mechanical tunneling in the Ado(*) and 8-MeOAdo(*)-mediated H(*) abstraction reactio

262 modeling before the structure was known, the Ado ligand lies over the southern quadrant of the molecu

263 e were also cleaved, with 43% and 32% of the Ado activity, respectively.

264 s indicate that the long, alkyl chain of the Ado amino acid imbeds into the lipid surface.

265 olecular mechanics (MM), and rotation of the Ado ligand relative to the corrin gave rise to four loca

266 e (Ade) moiety relative to the ribose of the Ado ligand.

267 s process is coupled to repositioning of the Ado moiety of AdoCbl from the eastern conformation to th

268 oxicity was prevented by the addition of the Ado transport inhibitor dipyridamole or the Ado kinase i

269 The growth inhibition of the Ado/CF combination was not abrogated by pyrimidines or c

270 sine dialdehyde) potentiated toxicity of the Ado/CF combination.

271 ribose and increased "strain" energy on the Ado group and to a lesser extent the corrin ring.

272 Ado transport inhibitor dipyridamole or the Ado kinase inhibitor 5'-amino 5'-deoxyadenosine.

273 Together, these findings indicate that the Ado-mediated killing proceeds via an intracellular route

274 In vitro studies further clarified that the Ado-Met binding domain of PRMT2 induces STAT3 methylatio

275 to four locally minimum structures with the Ado in the southern, eastern, northern, or western quadr

276 southern conformation is populated with the Ado ligand confined to an arc from over C15 to over C12,

277 None of these Ado receptor antagonists prevented capsaicin-induced C f

278 lammatory effect of CHA was mediated through Ado receptors since the effect was reversed by coadminis

279 ggest that hHcys decreases plasma and tissue Ado concentrations associated with inhibition of SAH hyd

280 Decrease in plasma and tissue Ado may be an important mechanism mediating the pathogen

281 enic effects by decrease in plasma or tissue Ado concentrations.

282 lated Meisenheimer complex of adenosine (TNP-Ado) in water were examined in the presence of alpha-, b

283 ent trinitrophenylated complexes of Ado (TNP-Ado) and Ino (TNP-Ino).

284 ith formation of a tight complex between TNP-Ado and gamma-CD.

285 eve detection limits of 32 and 38 nM for TNP-Ado and TNP-Ino, respectively.

286 is able to accommodate the TNP moiety of TNP-Ado.

287 The TNP-Ado complex exhibits minimal fluorescence in water, wher

288 The structure of the TNP-Ado:gamma-CD complex was determined by 2D nuclear magnet

289 The cocrystal structure of Fhit bound to Ado-p-CH2-p-ps-Ado (IB2), a nonhydrolyzable ApppA analog

290 The brief exposure to Ado was sufficient to observe inhibition of TCR-triggere

291 In the current work, two Ado cleavage activities were identified from M. smegmati

292 ded ADK is in an open conformation, and upon Ado binding a lid domain of the protein undergoes a larg

293 or control point for NFkappaB activation via Ado signaling.

294 , and substrate inhibition was observed when Ado concentrations exceeded 5 micro M.

295 xist and that slower growth occurs only when Ado/Aar are overexpressed at 38 degrees C.

296 fine a molecular regulatory pathway by which Ado provides potent antiinflammatory properties.

297 While Ado was the preferred substrate, inosine and guanosine w

298 so hypothesized that inhibition of ICMT with Ado/HC or AGGC might cause endothelial apoptosis by alte

299 ent K(m) (K(m) ( app)) of 98 +/- 6 muM (with Ado) and a native molecular mass of 125 +/- 7 kDa.

300 hout provoking the hypotension observed with Ado.