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 stacks against the conserved phenylalanine and form

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

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

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

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

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

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

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

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

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

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

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

15 ation of cytoplasmic cAMP with forskolin and IBMX.

16 perilipin upon incubation with forskolin and IBMX.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

32 enosine production that was not prevented by IBMX.

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

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

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

36 ',5'-dideoxyadenosine but were unaffected by IBMX.

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

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

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

40 01, Niflumic acid) and agonists (Forskolin + IBMX, UTP).

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

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

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

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

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

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

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

48 stable following stimulation with forskolin/IBMX/genistein.

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

50 However, IBMX induced a sustained endothelium-independent approxi

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

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

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

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

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

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

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

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

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

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

61 8-Br-cAMP or the phosphodiesterase inhibitor IBMX, suggesting high phosphodiesterase activity of CSQ

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

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

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

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

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

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

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

69 e presence of a phosphodiesterase inhibitor, IBMX.

70 Intracellular IBMX enhanced the photoresponse with little effect on th

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

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

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

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

75 FTR by forskolin and isobutylmethylxanthine (IBMX).

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

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

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

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

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

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

82 1 preadipocytes with isobutylmethylxanthine (IBMX), dexamethasone, and insulin, alone or in combinati

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

84 1-Methyl-3-isobutylxanthine (IBMX), a nonspecific phosphodiesterase (PDE) inhibitor,

85 8-Br-cGMP, 1-methyl-3-isobutylxanthine (IBMX), and atrial natriuretic peptide (ANP) but not 8-Br

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

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

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

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

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

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

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

93 3-Isobutyl-1-methylxanthine (IBMX) or 8-bromoadenosine 3',5'-cyclic monophosphate (8-

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

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

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

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

98 3-Isobutyl-1-methylxanthine (IBMX), a non-specific phosphodiesterase inhibitor, poten

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 ulated by an inhibitor of phosphodiesterase (IBMX).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 icantly alter the catalytic activity and the IBMX inhibition.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

182 iesterase inhibitor isobutylmethyl xanthine (IBMX).

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

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

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

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