ライフサイエンスコーパス: IBMX

1 IBMX arrests oocyte maturation, but Mos (or MEK) overexp

2 IBMX binds to a subpocket that comprises key residues Il

3 IBMX inhibits breakdown of cAMP and thus activates prote

4 IBMX stacks against the conserved phenylalanine and form

5 IBMX, an inhibitor of cAMP phosphodiesterase, had no sig

6 lutamate) and/or a protein kinase activator (IBMX, forskolin, TPA).

7 ion by itself and in concert with additional IBMX-sensitive PDEs.

8 ription induced by BMP2+cAMP-elevating agent IBMX, transient transfections of hPhox2a-reporter constr

9 Neither cAMP-inducing agent IBMX (0.01 mM and 0.1 mM) nor forskolin (0.001 mM) inhib

10 Application of 8-CPT-cAMP and IBMX did not mimic or prevent the effects of Som.

11 thyl-xanthine (IBMX) or with 8-pCPT-cGMP and IBMX together, indicating that PDE is not required for m

12 ntiated by sequential treatment with dex and IBMX displayed insulin sensitivity equivalent to DIM adi

13 the simultaneous treatment of forskolin and IBMX appeared to saturate sensitivity of melatonin synth

14 he broad range of effects that forskolin and IBMX can elicit through the intracellular second messeng

15 n response to a combination of forskolin and IBMX followed by genistein.

16 Treating isolated DCTs with forskolin and IBMX increased NCC phosphorylation via a protein kinase

17 show that neural induction by forskolin and IBMX is dependent on downregulation of expression of the

18 Forskolin and IBMX preserved the MMP, whereas both EPAC inhibitors dim

19 Both forskolin and IBMX prevented diclofenac-induced apoptosis.

20 ferentiation, it suggests that forskolin and IBMX result in transdifferentiation of MSCs into a neura

21 oplets in cells incubated with forskolin and IBMX, indicating that the addition of a negative charge

22 hat the cAMP-elevating agents, forskolin and IBMX, induced neural-like differentiation of MSCs, inclu

23 perilipin upon incubation with forskolin and IBMX.

24 ation of cytoplasmic cAMP with forskolin and IBMX.

25 ished the protective effect of forskolin and IBMX.

26 Basal, forskolin- and IBMX-stimulated cAMP content was significantly smaller i

27 Indomethacin (Indo, 2.5 microM) and IBMX (0.1 mM) were added 10 minutes before the addition

28 ry subunit of Protein Kinase A (RIalpha) and IBMX-bound phosphodiesterase8 (PDE8), monitored by amide

29 For PDE5(Q817A), vardenafil, sildenafil, and IBMX inhibitory potencies were weakened 610-, 48-, and 6

30 osine 3':5'-cyclic monophospate sodium), and IBMX (3-isobutyl-1-methylxanthine) also changed the spli

31 Although BMP2+IBMX increased endogenous Phox2a expression, the 7.5-kb

32 eacetylase inhibitor trichostatin A and BMP2+IBMX display increased endogenous Phox2a transcription a

33 luorescent protein were unresponsive to BMP2+IBMX, but active in both cell types.

34 Additionally, both IBMX and adenosine deaminase reduced ethanol-induced IR-

35 s also increased by PIA but was decreased by IBMX and adenosine deaminase.

36 the endothelium to the media was enhanced by IBMX or 8-bromo-cAMP, but not by 8-bromo-cGMP, whereas G

37 that treatment with dex for 48 h followed by IBMX treatment for 48 h was sufficient for adipogenesis,

38 essed by DIM or by dex-then-IBMX, but not by IBMX-then-dex treatment.

39 ter (PMA) in Raw264.7 monocytes, but only by IBMX in 3T3-L1 preadipocytes.

40 bited by H-89 and PD98059 and potentiated by IBMX and cholera toxin (250 microg/mL).

41 enosine production that was not prevented by IBMX.

42 ereas higher cAMP concentrations produced by IBMX and forskolin activate the more dominant cAMP-GEF p

43 Distal promoter activity was stimulated by IBMX and phorbol ester (PMA) in Raw264.7 monocytes, but

44 TR stimulation by forskolin, but not that by IBMX.

45 ',5'-dideoxyadenosine but were unaffected by IBMX.

46 ort HCMV reactivation from latency upon cAMP/IBMX treatment.

47 ate VIP and mACh receptors; VIP, with either IBMX or forskolin, activates the adenylyl cyclase pathwa

48 in strips partially denuded of endothelium, IBMX enhanced the transmission of hyperpolarization from

49 nt describing the decay in current following IBMX stimulation was surprisingly little affected by sub

50 01, Niflumic acid) and agonists (Forskolin + IBMX, UTP).

51 enhanced rescue and 2-fold higher forskolin+IBMX-activated currents of both I507-ATT and I507-ATC De

52 a are sufficient for activation by forskolin/IBMX, and this is accompanied by an increase in receptor

53 on of apical exocytosis (2 min) by forskolin/IBMX.

54 R alpha and ER beta sufficient for forskolin/IBMX activation, and the effect of cAMP on receptor phos

55 FTR(inh)-172 and in the absence of forskolin/IBMX (F/I); this decrease is interpreted as a measure of

56 d this correlates with the lack of forskolin/IBMX stimulated transcriptional activity.

57 eased by 3-fold in the presence of forskolin/IBMX.

58 taF508-CFTR with ENaC enhanced the forskolin/IBMX/genistein-mediated activation of DeltaF508-CFTR.

59 stable following stimulation with forskolin/IBMX/genistein.

60 However, the FSK/IBMX-induced potentiation in cells loaded with the speci

61 However, IBMX induced a sustained endothelium-independent approxi

62 Treatment with combined factors (aFGF+5-HT+IBMX+forskolin+TPA) yielded the greatest level of TPH in

63 both Pde3b promoter regions was increased in IBMX-treated preadipocytes.

64 r not the low-Ca(2+)-O Na+ solution included IBMX.

65 uced distal promoter activity; H89 inhibited IBMX-stimulated CREB phosphorylation and proximal and di

66 ermore, the nonisoformspecific PDE inhibitor IBMX and PDE5-specific inhibitors suppressed IL-1-induce

67 P (5 mM) and the phosphodiesterase inhibitor IBMX (0.5 mM) prevented the decrease in relative express

68 plication of the phosphodiesterase inhibitor IBMX increased fluorescence in the cilia and other neuro

69 Thus, the phosphodiesterase inhibitor IBMX promotes the actions of HCO(3)(-) on flagellar and

70 administered the phosphodiesterase inhibitor IBMX to animals treated with eticlopride.

71 exposure to the phosphodiesterase inhibitor IBMX to monitor indirectly the decay in intraciliary Ca(

72 skolin), the pan-phosphodiesterase inhibitor IBMX, and EPAC inhibitors 5,7-dibromo-6-fluoro-3,4-dihyd

73 8-Br-cAMP or the phosphodiesterase inhibitor IBMX, suggesting high phosphodiesterase activity of CSQ

74 nifedipine, the phosphodiesterase inhibitor IBMX, the adenylyl cyclase activator forskolin, or the P

75 of cAMP and the phosphodiesterase inhibitor IBMX, we show that PKA activity is required for AR induc

76 levated by the phospho-diesterase inhibitor, IBMX, suggesting OMP acts upstream of cAMP production.

77 specific phosphodiesterase enzyme inhibitor, IBMX (100 microM), implicating the importance of intrace

78 inhibited by the non-specific PDE inhibitor, IBMX.

79 nt with a phosphodiesterase (PDE) inhibitor, IBMX, which increases intraoocyte cAMP levels.

80 ked by a potent phosphodiesterase inhibitor, IBMX (3-isobutyl-1-methylxanthine).

81 e presence of a phosphodiesterase inhibitor, IBMX.

82 Intracellular IBMX enhanced the photoresponse with little effect on th

83 um PDE inhibitor, 3'-isobutylmethylxanthine (IBMX), produced a 9-fold increase in the cAMP level, dou

84 sterase inhibitor, 3-isobutylmethylxanthine (IBMX), inhibited urea synthesis albeit increased [cAMP].

85 n, 8-bromo cAMP, and isobutylmethylxanthine (IBMX) all prevented CD47-mediated apoptosis, indicating

86 s with forskolin and isobutylmethylxanthine (IBMX) to elevate levels of cAMP and activate protein kin

87 FTR by forskolin and isobutylmethylxanthine (IBMX).

88 receptor antagonist isobutylmethylxanthine (IBMX) or with adenosine uptake inhibitor adenosine deami

89 diesterase inhibitor isobutylmethylxanthine (IBMX) or the cell permeant cAMP analog 8-bromo-cAMP, rel

90 diesterase inhibitor isobutylmethylxanthine (IBMX) to promote cell death in 3T3-L1 preadipocytes plac

91 diesterase inhibitor isobutylmethylxanthine (IBMX; 10 microM), the non-hydrolysable cAMP analogue 8-b

92 in (Fsk; 1 microm) + isobutylmethylxanthine (IBMX; 100 microm), which elevates cellular cAMP, trigger

93 iously reported that isobutylmethylxanthine (IBMX), a derivative of oxypurine, inhibits citrulline sy

94 1 preadipocytes with isobutylmethylxanthine (IBMX), dexamethasone, and insulin, alone or in combinati

95 ombination with 1-Methyl-3-isobutylxanthine (IBMX) induced a long-lasting synaptic enhancement at MF

96 1-Methyl-3-isobutylxanthine (IBMX), a nonspecific phosphodiesterase (PDE) inhibitor,

97 8-Br-cGMP, 1-methyl-3-isobutylxanthine (IBMX), and atrial natriuretic peptide (ANP) but not 8-Br

98 ion with 16.7 mmol/l glucose plus 0.1 mmol/l IBMX caused a biphasic secretion of human IAPP-LI and mo

99 target specificities. Of interest, measured IBMX-dependent cAMP levels were an order of magnitude hi

100 diesterase inhibitor methylisobutylxanthine (IBMX) and fetal bovine serum (FBS).

101 a complex with 3-isobutyl-1-methylxanthine (IBMX) at 1.55 A resolution.

102 ctive inhibitor 3-isobutyl-1-methylxanthine (IBMX) binds to a similar subpocket in the active sites o

103 unliganded and 3-isobutyl-1-methylxanthine (IBMX) bound forms at 1.9 and 2.1 A resolutions, respecti

104 (PDE) inhibitor 3-isobutyl-1-methylxanthine (IBMX) did not elevate cGMP on its own but consistently a

105 orskolin and/or 3-isobutyl-1-methylxanthine (IBMX) in light-dark (LD) and DD.

106 eased effect of 3-isobutyl-1-methylxanthine (IBMX) observed in GADA+ donor islets.CONCLUSIONWe found

107 3-Isobutyl-1-methylxanthine (IBMX) or 8-bromoadenosine 3',5'-cyclic monophosphate (8-

108 ither forskolin/3-isobutyl-1-methylxanthine (IBMX) or the V2 receptor agonist [deamino-Cys(1),d-Arg(8

109 rskolin, and/or 3-isobutyl-1-methylxanthine (IBMX) to determine whether these agents, alone or in com

110 , tadalafil, or 3-isobutyl-1-methylxanthine (IBMX) were respectively weakened 14-, 123-, 30-, 51-, an

111 the presence of 3-isobutyl-1-methylxanthine (IBMX), 10 microM SNC was sufficient to induce cGMP-IR, a

112 3-Isobutyl-1-methylxanthine (IBMX), a non-specific phosphodiesterase inhibitor, poten

113 Moreover, 3-isobutyl-1-methylxanthine (IBMX), an inhibitor of cAMP phosphodiesterase, potentiat

114 ine, 0.1 mmol/l 3-isobutyl-1-methylxanthine (IBMX), and 5 micromol/l carbachol induced a >50-fold inc

115 reasing agents, 3-isobutyl-1-methylxanthine (IBMX), and forskolin completely abolished palmitate-medi

116 PDE inhibitor, 3-isobutyl-1-methylxanthine (IBMX), and the PDE3 selective inhibitors milrinone and c

117 erase inhibitor 3-isobutyl-1-methylxanthine (IBMX), decreased the period (increased the frequency) of

118 erase inhibitor 3-isobutyl-1-methylxanthine (IBMX), the circulating current was restored.

119 f forskolin and 3-isobutyl-1-methylxanthine (IBMX), we show that increase of cAMP resulted in inhibit

120 forskolin plus 3-isobutyl-1-methylxanthine (IBMX), which increases intracellular cAMP, stimulated th

121 able, forskolin+3-isobutyl-1-methylxanthine (IBMX)-activated whole-cell currents in the presence of t

122 rase inhibitor, 3-isobutyl-1-methylxanthine (IBMX).

123 erase inhibitor 3-isobutyl-1-methylxanthine (IBMX).

124 kolin (FSK) and 3-isobutyl-1-methylxanthine (IBMX).

125 ogenic inducer, 3-isobutyl-1-methylxanthine (IBMX).

126 sildenafil, and 3-isobutyl-1-methylxanthine (IBMX).

127 erase inhibitor 3-isobutyl-1-methylxanthine (IBMX, 750 microM) reversibly increased the IPSCs as well

128 s with PDGF and 3-isobutyl-1-methylxanthine (IBMX, a phosphodiesterase inhibitor) enhanced the accumu

129 toisocaproate-, 3-isobutyl-1-methylxanthine (IBMX-), KCl-, and tolbutamide-induced insulin secretion.

130 potentiated by 3-isobutyl-1-methylxanthine (IBMX; phosphodiesterase type 5 inhibitor and adenosine a

131 the effects of 1-isobutyl-3-methylxanthine (IBMX) and forskolin, agonists that elevate cAMP in these

132 esterase inhibitor, isobutyl methylxanthine (IBMX) increased the potency of PACAP at inducing neurite

133 hibitors, e.g. 3-isobutyl-1-methylxanthine [(IBMX) or caffeine, 10 mg/kg] or the more specific cAMP-P

134 respectively) or 100 microM SNAP + 10 microM IBMX (EC(50) = 10 microM and 8.2 nM, respectively).

135 respectively) or 100 microM SNAP + 10 microM IBMX (EC(50) = 9 microM and 8.4 nM, respectively).

136 y cAMP cocktail (250 microM cAMP, 100 microM IBMX, and 25 microM forskolin) and were inhibited by 1 m

137 mine-NO (200 microm), milrinone (10 microm), IBMX (100 microm) or forskolin (1 microm) was significan

138 ays utilizing pure enzyme showed that 0.2 mM IBMX completely inhibited PDE activity.

139 ntation, motility, and responsiveness to MSH/IBMX, a behavior similar to that recently reported for a

140 eceptors were disabled by ryanodine, neither IBMX nor milrinone was able to amplify LCRs, accelerate

141 The nondifferentiating IBMX-then-dex treatment produced transient expression of

142 deomicroscopy in the presence and absence of IBMX, an inhibitor of cAMP phosphodiesterase.

143 The protective action of IBMX and forskolin was rapid and did not appear to requi

144 In the presence of BAPTA-AM, the actions of IBMX were reduced.

145 The addition of IBMX or dbcAMP to indomethacin-treated, UVB-exposed cell

146 The combined administration of IBMX and eticlopride induced gene expression that was on

147 ay suggest a new experimental application of IBMX in studies of CPS-I malfunction and the use of agma

148 Surprisingly, intracellular application of IBMX or of the second messenger cAMP via the patch pipet

149 In contrast, extracellular application of IBMX produced a rapid and reversible inhibition of THIK-

150 -1 currents were inhibited by application of IBMX with an IC(50) of 120 uM.

151 so inhibited by extracellular application of IBMX.

152 ites did not change the inhibitory effect of IBMX on THIK-1 currents.

153 1, markedly reduced the inhibitory effect of IBMX.

154 yryl-cAMP mimicked the protective effects of IBMX and forskolin, suggesting that cAMP is the mediator

155 pathway, mimicked the protective effects of IBMX and forskolin, suggesting that the cAMP-GEF pathway

156 utions of the different functional groups of IBMX based on their interactions with the orthosteric re

157 The unfavorable interaction of IBMX in the PDE8A1-IBMX structure suggests an important

158 y different orientations and interactions of IBMXs are observed among the three PDE families and also

159 Among various oxypurines tested, only IBMX, xanthine, or uric acid significantly increased the

160 llowing treatment with forskolin, 8BrcAMP or IBMX rescued cells from SNP-induced cell death.

161 n of intact beta TC3 cells with forskolin or IBMX resulted in the phosphorylation of the cardiac-type

162 however, the ability of either forskolin or IBMX to potentiate glucose-induced insulin secretion was

163 ebellar slices, treatment with sildenafil or IBMX led to different levels of phospho-PDE5 accumulatio

164 ffinity for cGMP, vardenafil, sildenafil, or IBMX in Y612F, H613A, L765A, or F786A was less, but affi

165 cGMP, vardenafil, sildenafil, tadalafil, or IBMX was reduced 5.5-, 23-, 10-, 3-, and 12-fold, respec

166 nfavorable interaction of IBMX in the PDE8A1-IBMX structure suggests an important role of Tyr748 in t

167 rskolin (10 microm) or the phosphodiesterase IBMX (50 microm) enhanced (39-42%) agonist-evoked NO rel

168 ulated by an inhibitor of phosphodiesterase (IBMX).

169 t specific inhibitors of phosphodiesterases (IBMX) and CD73 (AMPCP) were determined by high-pressure

170 ion, while inhibition of phosphodiesterases (IBMX, 100 microm) shifted I(f) activation in the depolar

171 and (2) the addition of dibutyryl cAMP plus IBMX.

172 antagonist, microinjection of forskolin plus IBMX decreased the period to 66 % of baseline levels.

173 ting indicated that in 3T3-L1 preadipocytes, IBMX-stimulated induction of Pde3b mRNA and protein was

174 In addition, agmatine may prevent IBMX from binding to one or more active site(s) of CPS-I

175 r PPARgamma ectopic expression nor prolonged IBMX treatment rescued defects in Prdm16 expression in D

176 efore and after application of SNAP or SNAP+ IBMX.

177 was determined before and after SNAP or SNAP+IBMX.

178 Here, we demonstrate that IBMX and other oxypurines containing a 2,6-dione group i

179 The results demonstrate that IBMX induced the following: (i) inhibition of the mitoch

180 , alone or in combination, demonstrated that IBMX, which increased cAMP-response element-binding prot

181 Thus, we hypothesized that IBMX inhibits hepatic urea synthesis independent of [cAM

182 The results indicate that IBMX directly and specifically inhibited complex I of th

183 round light or after bleaches, provided that IBMX was used to restore sufficient photocurrent so that

184 Our results suggest that IBMX binds directly to the channel and that the inhibiti

185 icantly alter the catalytic activity and the IBMX inhibition.

186 her theorized that agmatine would negate the IBMX action and improve ureagenesis.

187 DE8A1 catalytic domain is insensitive to the IBMX inhibition (IC(50) = 700 microM).

188 ylate cyclase activity was measured with the IBMX (3-isobutyl-1-methylxanthine) jump technique.

189 (Pref-1) was repressed by DIM or by dex-then-IBMX, but not by IBMX-then-dex treatment.

190 r to that seen when returning immediately to IBMX-free Ringer solution.

191 ole to inhibit the response of other ORNs to IBMX (3-isobutyl-1-methylxanthine)/forskolin in a PI3K-d

192 minates the falling phase of the response to IBMX, which can therefore be used to assess exchanger ac

193 in secretion (GSIS) and insulin secretion to IBMX and KCl were all reduced without altering oxygen co

194 er of co-activator molecules (dopamine, TPA, IBMX/forskolin), will induce the expression of the catec

195 prisingly, THIK-1 current was inhibited when IBMX was applied from the extracellular side of the memb

196 ctivity by an additional 2.5-3-fold, whereas IBMX alone was essentially without effect.

197 In) to 84 % (without IBMX) and to 72 % (with IBMX) of the pre-injection baseline.

198 Perfusion of agmatine with IBMX stimulated O(2) consumption, restored hepatic phosp

199 vating cyclic nucleotide levels, either with IBMX or by application of either Bt2cAMP (EC50 = 14.7 mi

200 Experiments with IBMX have shown that 1), sustained cAMP elevation is mor

201 Incubation with IBMX (2 x 10(-4) M) significantly elevated cAMP in both

202 ted by inhibition of phosphodiesterase (with IBMX) or adenylate cyclase (with SQ22536) or by raising

203 while inhibition of phosphodiesterases with IBMX (100 mum) increased I(CaL) amplitude.

204 ent for adipogenesis, whereas treatment with IBMX followed by dex failed to induce significant differ

205 he hypoglossal nerve (XIIn) to 84 % (without IBMX) and to 72 % (with IBMX) of the pre-injection basel

206 iesterase inhibitor isobutylmethyl xanthine (IBMX).

207 Forskolin or 3-isobutyl-1-methyl xanthine (IBMX), 2 inducers of adenylate cyclase, markedly enhance

208 The effects of isobutyl methyl xanthine (IBMX), an inhibitor of phosphodiesterase and of dibutyry

209 activation by 3-isobutyl 1-methyl xanthine (IBMX), as expected if these TMs are intimately involved

210 rase inhibitor 3-isobutyl-1-methyl-xanthine (IBMX) as a pharmacological tool to induce activation of

211 the effect of 3-isobutyl-1-methyl-xanthine (IBMX) on THIK-1 currents.

212 PDE inhibitor 3-isobutyl-1-methyl-xanthine (IBMX) or with 8-pCPT-cGMP and IBMX together, indicating