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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

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