ライフサイエンスコーパス: methylxanthine

1 sphodiesterase inhibitor, IBMX (3-isobutyl-1-methylxanthine).

2 CFTR activation with forskolin/3-isobutyl-1-methylxanthine.

3 taF508 channel activity by 2 mm 3-isobutyl-1-methylxanthine.

4 or specificity change from theophylline to 3-methylxanthine.

5 itors, sildenafil, or zaprinast 3-isobutyl-1-methylxanthine.

6 the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine.

7 g the nonspecific PDE inhibitor 3-isobutyl-1-methylxanthine.

8 rskolin, 1 mmol/l 8-Br-cAMP, or 3-isobutyl-1-methylxanthine.

9 lthio-cAMP, dibutyryl-cAMP, and 3-isobutyl-1-methylxanthine.

10 n kinase A such as forskolin or 3-isobutyl-1-methylxanthine.

11 iction but not glibenclamide or 3-isobutyl-1-methylxanthine.

12 after stimulation by forskolin/3-isobutyl-1-methylxanthine.

13 nitrogen sources but also theophylline and 3-methylxanthine.

14 ere further N demethylated to xanthine via 7-methylxanthine.

15 ntain caffeine, a pharmaceutically important methylxanthine.

16 nolayers treated with forskolin/3-isobutyl-1-methylxanthine.

17 the arrest with chemical compounds known as methylxanthines.

18 ious studies, placing particular emphasis on methylxanthines.

19 concentrations of CF-derived metabolites and methylxanthines.

20 ia a hitherto unreported pathway to 1- and 3-methylxanthines.

21 re is a resurgence of interest in the use of methylxanthines.

22 l cross reactivity with structurally related methylxanthines.

23 cAMP) (forskolin (1-10 microM), 3-isobutyl-1-methylxanthine (0.1-1 mM), rolipram (10 microM), and dib

24 us amounts of cocoa flavanols (0-820 mg) and methylxanthines (0-220 mg), either together or individua

25 ment was assessed by metabolism of infused 1-methylxanthine (1-MX) and by contrast-enhanced ultrasoun

26 protocol 2 subjects, tissue extraction of 1-methylxanthine (1-MX) was measured as an index of perfus

27 as assessed by measuring the metabolism of 1-methylxanthine (1-MX), an exogenously added substrate fo

28 io) (8-CPT)-cAMP (100 micromol/L) + isobutyl methylxanthine (100 micromol/L).

29 ol myristic acid, forskolin and 3-isobutyl-1-methylxanthine, 2) BPDZ 154, or 3) 4-phenylbutyrate.

30 C(50) values for the inhibitors 3-isobutyl-1-methylxanthine (20 microM) and sildenafil (Viagra(TM))(4

31 f forskolin (20 micromol/L) and 3-isobutyl-1-methylxanthine (20 micromol/L), also inhibited GCDC-indu

32 osphodiesterase (PDE) inhibitor 3-isobutyl-1-methylxanthine (20 mumol/L).

33 the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (5x10(-5) mol/L).

34 hine, and 1-methylxanthine to theobromine, 3-methylxanthine, 7-methylxanthine, and xanthine, respecti

35 t polyphenols, whereas caffeine was the main methylxanthine (90%).

36 zene sulphonate (21 microM) and 3-isobutyl-1-methylxanthine (970 microM, partial inhibition) were als

37 was enhanced in the presence of 3-isobutyl-1-methylxanthine, a cAMP phosphodiesterase inhibitor.

38 ydig cells from wild-type mice, 3-isobutyl-1-methylxanthine, a compound that inhibits all cAMP PDEs e

39 has been proposed that caffeine and related methylxanthines activate taste-receptor cells through in

40 newborns respond adequately to, or tolerate, methylxanthine administration, and thus alternative phar

41 Oral or intravenous methylxanthine agents may be given for more severe PDPH.

42 activating CFTR with forskolin/3-isobutyl-1-methylxanthine alkalinized NL ASL but acidified CF ASL;

43 monophospate sodium), and IBMX (3-isobutyl-1-methylxanthine) also changed the splicing pattern.

44 In the presence of Mg(2+), methylxanthines altered the structure of DNA from B to A

45 ed by 2',5'-dideoxyadenosine or 3-isobutyl-1-methylxanthine, an inhibitor of phosphodiesterase.

46 1-Methylxanthine and 3-methylxanthine were subsequently N

47 of matched doses (300 nmol) of 3-isobutyl-1-methylxanthine and 7-deacetyl-7-O-(N-methylpiperazino)-g

48 y by the nonselective PDE inhibitor isobutyl methylxanthine and also by the selective PDE 3B inhibito

49 ese effects were potentiated by 3-isobutyl-1-methylxanthine and attenuated by the adenylyl cyclase in

50 intracellular cAMP prompted by 3-isobutyl-1-methylxanthine and forskolin partially mimicked the effe

51 However, 3-isobutyl-1-methylxanthine and forskolin treatment of a muscle that

52 ex with non-selective inhibitor 3-isobutyl-1-methylxanthine and kinetic analysis on the mutants of PD

53 d) complexed with sildenafil or 3-isobutyl-1-methylxanthine and the Pgamma-inhibitory peptide Pgamma(

54 microM forskolin and 300 microM 3-isobutyl-L-methylxanthine and voltage-clamped with pipettes contain

55 Release was also stimulated by 3-isobutyl-1-methylxanthine and was additive with forskolin.

56 rdenafil or sildenafil (but not 3-isobutyl-1-methylxanthine and zaprinast) induced a distinct conform

57 extraction methods for the determination of methylxanthines and tannins were investigated.

58 (MEF-KO) impairs dexamethasone, 3-isobutyl-1-methylxanthine, and insulin (DMI)-induced adipocyte diff

59 se [cAMP] (forskolin, rolipram, 3-isobutyl-1-methylxanthine, and papaverine) or mimic cAMP (8-bromo-c

60 d was mimicked by 8-bromo-cAMP, 3-isobutyl-1-methylxanthine, and Sp-cAMP.

61 he phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, and the adenylate cyclase activator, for

62 xanthine to theobromine, 3-methylxanthine, 7-methylxanthine, and xanthine, respectively.

63 R2 by the same mechanism as phosphorylation, methylxanthines, and mutations, via changes in the thres

64 ration of adenosine antagonists, such as the methylxanthines antagonists caffeine and theophylline, o

65 ed mTOR in vitro, demonstrating that certain methylxanthines are able to inhibit mTOR independently o

66 the 8'-methyl carbinols of these N7-methyl-8-methylxanthines are formed in substantial amounts with e

67 By contrast, the N7-methyl-8-methylxanthines are good substrates for CYP1A2 but are n

68 y caffeine, theobromine, paraxanthine, and 7-methylxanthine as sole carbon and nitrogen sources but a

69 Vpr-mediated G2 arrest was alleviated by methylxanthines at concentrations similar to those neede

70 2 [(E)-1,3-diethyl-8-(3,4-dimethoxystyryl)-7-methylxanthine], both in normal and in dopamine-depleted

71 t beneficial: 16,607 (24%) were treated with methylxanthine bronchodilators, 10,051 (14%) had sputum

72 We have previously reported that the methylxanthine caffeine increases expression of the spli

73 In both types of organisms, the methylxanthine caffeine overrides the synthesis (S)-M ch

74 and Mexican Northwest reveal combinations of methylxanthines (caffeine, theobromine, and theophylline

75 talyzed N(3)-demethylation of theobromine, 3-methylxanthine, caffeine, and theophylline to 7-methylxa

76 were no differences in circulating levels of methylxanthines, catecholamines, or glucose.

77 10 microm forskolin, 40 microm 3-isobutyl-1-methylxanthine caused a 50% reduction in myosin II regul

78 the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine, caused a rightward shift in the current-

79 ructures together with the PDE5A1-isobutyl-1-methylxanthine complex show that the H-loop (residues 66

80 er shows less heterogeneity in the aptamer-3-methylxanthine complex than what is observed in the theo

81 y structure of DNA remained unaltered in DNA-methylxanthines complexes or in the absence of Mg(2+).

82 ferent brewing methods on the polyphenol and methylxanthine composition and antioxidant capacity of t

83 mportant source of polyphenols with moderate methylxanthines content; therefore its high antioxidant

84 of methyl group substitutions on the 1- or 3-methylxanthine core structure.

85 ot to act on the cyclase, or by 3-isobutyl-1-methylxanthine, creatine phosphate, or creatine kinase.

86 esent study demonstrates that theobromine, a methylxanthine derivative present in cocoa, effectively

87 under identical culture conditions (isobutyl-methylxanthine, dexamethasone, and insulin), revealed mu

88 n tyrosinase activity by either 3-isobutyl-1-methylxanthine, dibutyryl cAMP, or forskolin.

89 ets perifused with glucose and 3-isobutryl-1-methylxanthine did not respond to glucose deprivation by

90 ombination of dexamethasone and 3-isobutyl-1-methylxanthine (DM) is suppressed by 2,3,7,8 tetrachloro

91 howed 24-35% of enhanced binding activity of methylxanthines during helix-coil transitions of DNA rat

92 l ester hydrochloride (T-0156), 3-isobutyl-1-methylxanthine, EDTA, or cGMP, but not by cAMP or 5'-GMP

93 tial interaction between cocoa flavanols and methylxanthines exists at the level of absorption, in wh

94 r an interaction between cocoa flavanols and methylxanthines exists that influences cocoa flavanol-de

95 response of other ORNs to IBMX (3-isobutyl-1-methylxanthine)/forskolin in a PI3K-dependent manner arg

96 ytochrome P450 1A2) activity caused by the 8-methylxanthine furafylline is investigated with the aim

97 However, 3-methylxanthine-grown CBB5 cells did not metabolize caffe

98 Theobromine-, paraxanthine-, and 7-methylxanthine-grown cells also metabolized all of the m

99 lin, 1 mM 8-bromo-cAMP, or 1 mM 3-isobutyl-1-methylxanthine) had no effect on the amplitude of Kv1.5

100 with the nonselective inhibitor 3-isobutyl-1-methylxanthine have been determined at medium resolution

101 We have examined the effects of 1-isobutyl-3-methylxanthine (IBMX) and forskolin, agonists that eleva

102 tal structure as a complex with 3-isobutyl-1-methylxanthine (IBMX) at 1.55 A resolution.

103 The nonselective inhibitor 3-isobutyl-1-methylxanthine (IBMX) binds to a similar subpocket in th

104 tructures in the unliganded and 3-isobutyl-1-methylxanthine (IBMX) bound forms at 1.9 and 2.1 A resol

105 osphodiesterase (PDE) inhibitor 3-isobutyl-1-methylxanthine (IBMX) did not elevate cGMP on its own bu

106 y treated with forskolin and/or 3-isobutyl-1-methylxanthine (IBMX) in light-dark (LD) and DD.

107 ective phosphodiesterase inhibitor, isobutyl methylxanthine (IBMX) increased the potency of PACAP at

108 3-Isobutyl-1-methylxanthine (IBMX) or 8-bromoadenosine 3',5'-cyclic m

109 MP levels with either forskolin/3-isobutyl-1-methylxanthine (IBMX) or the V2 receptor agonist [deamin

110 P, carbachol, forskolin, and/or 3-isobutyl-1-methylxanthine (IBMX) to determine whether these agents,

111 afil, sildenafil, tadalafil, or 3-isobutyl-1-methylxanthine (IBMX) were respectively weakened 14-, 12

112 In the presence of 3-isobutyl-1-methylxanthine (IBMX), 10 microM SNC was sufficient to i

113 3-Isobutyl-1-methylxanthine (IBMX), a non-specific phosphodiesterase

114 Moreover, 3-isobutyl-1-methylxanthine (IBMX), an inhibitor of cAMP phosphodiest

115 10 mmol/l arginine, 0.1 mmol/l 3-isobutyl-1-methylxanthine (IBMX), and 5 micromol/l carbachol induce

116 ells to cAMP-increasing agents, 3-isobutyl-1-methylxanthine (IBMX), and forskolin completely abolishe

117 A nonselective PDE inhibitor, 3-isobutyl-1-methylxanthine (IBMX), and the PDE3 selective inhibitors

118 the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), decreased the period (increased t

119 the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), the circulating current was resto

120 sed by the use of forskolin and 3-isobutyl-1-methylxanthine (IBMX), we show that increase of cAMP res

121 t transfections, forskolin plus 3-isobutyl-1-methylxanthine (IBMX), which increases intracellular cAM

122 s, leading to stable, forskolin+3-isobutyl-1-methylxanthine (IBMX)-activated whole-cell currents in t

123 the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX).

124 ent with an adipogenic inducer, 3-isobutyl-1-methylxanthine (IBMX).

125 MP, vardenafil, sildenafil, and 3-isobutyl-1-methylxanthine (IBMX).

126 he phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (IBMX).

127 the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX, 750 microM) reversibly increased t

128 Incubating cells with PDGF and 3-isobutyl-1-methylxanthine (IBMX, a phosphodiesterase inhibitor) enh

129 n succinate-, ketoisocaproate-, 3-isobutyl-1-methylxanthine (IBMX-), KCl-, and tolbutamide-induced in

130 mol/L; >3-fold), potentiated by 3-isobutyl-1-methylxanthine (IBMX; phosphodiesterase type 5 inhibitor

131 ase (cAMP-PDE) inhibitors, e.g. 3-isobutyl-1-methylxanthine [(IBMX) or caffeine, 10 mg/kg] or the mor

132 tentials upon presentation of theobromine, a methylxanthine in cocoa.

133 sustained response to glucose plus isobutyl-methylxanthine in perifusion studies that is clearly lar

134 the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine in proportion to increases in intracellul

135 ed, as was the response to theophylline, the methylxanthine in tea.

136 the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine in the medium, suggesting extracellular c

137 3-isobutyl-1-methylxanthine increased insulin secretion but had littl

138 phosphodiesterase activity with 3-isobutyl-1-methylxanthine, indicating that alpha-adrenergic stimula

139 we have investigated the mechanisms by which methylxanthines induce this aberrant overexpression.

140 he broad-spectrum PDE inhibitor 3-isobutyl-1-methylxanthine induced T cell CREB phosphorylation, we t

141 tors for their ability to mimic 3-isobutyl-1-methylxanthine-induced ATF-1/CREB phosphorylation.

142 The receptor inhibitor 3-isobutyl-1-methylxanthine inhibited the calcium response to adenosi

143 Methylxanthine intake alone did not result in statistica

144 pathways converged at xanthine via different methylxanthine intermediates.

145 ity was measured with the IBMX (3-isobutyl-1-methylxanthine) jump technique.

146 s were randomized to receive the substituted methylxanthine, lisofylline (CT1501R), or an identically

147 sts at the level of absorption, in which the methylxanthines mediate an increased plasma concentratio

148 g treatment with these diols or 3-isobutyl-1-methylxanthine, melanin and tyrosinase activity are incr

149 hine-grown cells also metabolized all of the methylxanthines mentioned above via the same pathway.

150 Rgamma) by dexamethasone (DEX), 3-isobutyl-1-methylxanthine (MIX), and insulin.

151 eviously attributed to one broad-specificity methylxanthine N-demethylase composed of two subunits, N

152 th forskolin, 8-bromo-cAMP, and 3-isobutyl-1-methylxanthine or by overexpression of the catalytic sub

153 ucing novel products increasing polyphenols, methylxanthines or dietary fibre to improve purported he

154 3-Isobutyl-1-methylxanthine potentiated ATP-induced calcium transient

155 n inability to avoid caffeine or the related methylxanthine present in tea, theophylline.

156 Caffeine is a methylxanthine present in the coffee tree, tea plant, an

157 ith 8-bromo cAMP, forskolin, or 3-isobutyl-1-methylxanthine prevented the CD47-mediated apoptosis, an

158 Methylxanthines reduced extubation failure (RR, 0.48; 95

159 ethylxanthine, xanthine, paraxanthine, and 1-methylxanthine, respectively.

160 8.6 mg of total-dietary-fibre, flavanols and methylxanthines, respectively) as well as PPCP (providin

161 9.8 mg of total-dietary-fibre, flavanols and methylxanthines, respectively) on cardiovascular health

162 ake, the consumption of cocoa flavanols with methylxanthines resulted in a greater enhancement of FMD

163 tein kinase (PKA), MgATP, cGMP, 3-isobutyl-1-methylxanthine], shown earlier to produce Ser92 phosphor

164 ucts had similar affinities for 3-isobutyl-1-methylxanthine, sildenafil, tadalafil, and UK-122764, bu

165 Caffeine, a methylxanthine, slightly increased basal levels of cAMP,

166 The forskolin/3-isobutyl-1-methylxanthine-stimulated whole-cell conductance in hCFT

167 udied the interaction of naturally occurring methylxanthines such as theophylline, theobromine and ca

168 aptamer that binds with higher affinity to 3-methylxanthine than theophylline.

169 fter the co-ingestion of cocoa flavanols and methylxanthines than after the intake of cocoa flavanols

170 e obtained when pure (-)-epicatechin and the methylxanthines theobromine and caffeine were consumed t

171 However, cocoa also contains the methylxanthines theobromine and caffeine, which may also

172 caffeine, theophylline, paraxanthine, and 1-methylxanthine to theobromine, 3-methylxanthine, 7-methy

173 dent Rieske oxygenase for demethylation of 7-methylxanthine to xanthine, the final step in caffeine N

174 CBB5 also oxidized theophylline and 1- and 3-methylxanthines to 1,3-dimethyluric acid and 1- and 3-me

175 histamines, systemic glucocorticosteroids or methylxanthines to manage anaphylaxis.

176 alkaloids, metabolizes caffeine and related methylxanthines via sequential N-demethylation to xanthi

177 ndent conversion of theophylline to 1- and 3-methylxanthines was also detected in the crude cell extr

178 cGMP, and IC50 for zaprinast or 3-isobutyl-1-methylxanthine were found among wild-type and mutant cGB

179 1-Methylxanthine and 3-methylxanthine were subsequently N demethylated to xanth

180 was more pronounced when cocoa flavanols and methylxanthines were ingested together.

181 Polyphenols and methylxanthines were qualitatively and quantitatively an

182 Additionally, 46 polyphenols and 2 methylxanthines were quantified by HPLC-DAD.

183 is an enantiomer-specific, alkyl-substituted methylxanthine, which has specific and potent activity i

184 mbination of dibutyryl cAMP and 3-isobutyl-1-methylxanthine, which increase intracellular Ca2+ and cA

185 3-isobutyl-1-methylxanthine, which potentiates the cGMP/cAMP-signalin

186 t is most potently inhibited by 3-isobutyl-1-methylxanthine with an IC(50) of 2.1 microM.

187 hylxanthine, caffeine, and theophylline to 7-methylxanthine, xanthine, paraxanthine, and 1-methylxant

188 by ANP/BNP, or blocking PDE by 3-isobutyl-1-methylxanthine/zaprinast caused significant inhibition o