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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
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
34 hine, and 1-methylxanthine to theobromine, 3-methylxanthine, 7-methylxanthine, and xanthine, respecti
36 zene sulphonate (21 microM) and 3-isobutyl-1-methylxanthine (970 microM, partial inhibition) were als
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
42 activating CFTR with forskolin/3-isobutyl-1-methylxanthine alkalinized NL ASL but acidified CF ASL;
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
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
56 rdenafil or sildenafil (but not 3-isobutyl-1-methylxanthine and zaprinast) induced a distinct conform
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
61 he phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, and the adenylate cyclase activator, for
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
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
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
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
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
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
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
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
107 ective phosphodiesterase inhibitor, isobutyl methylxanthine (IBMX) increased the potency of PACAP at
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
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
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
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
136 the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine in the medium, suggesting extracellular c
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
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.
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
157 ith 8-bromo cAMP, forskolin, or 3-isobutyl-1-methylxanthine prevented the CD47-mediated apoptosis, an
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
167 udied the interaction of naturally occurring methylxanthines such as theophylline, theobromine and ca
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
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
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
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
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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