ライフサイエンスコーパス: 3-isobutyl-1-methylxanthine

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

2 KCl preconstriction but not glibenclamide or 3-isobutyl-1-methylxanthine.

3 incipal cells after stimulation by forskolin/3-isobutyl-1-methylxanthine.

4 racts from monolayers treated with forskolin/3-isobutyl-1-methylxanthine.

5 alone before CFTR activation with forskolin/3-isobutyl-1-methylxanthine.

6 nt of CFTRDeltaF508 channel activity by 2 mm 3-isobutyl-1-methylxanthine.

7 he PDE5 inhibitors, sildenafil, or zaprinast 3-isobutyl-1-methylxanthine.

8 presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine.

9 DE8, including the nonspecific PDE inhibitor 3-isobutyl-1-methylxanthine.

10 micromol/l forskolin, 1 mmol/l 8-Br-cAMP, or 3-isobutyl-1-methylxanthine.

11 , chlorophenylthio-cAMP, dibutyryl-cAMP, and 3-isobutyl-1-methylxanthine.

12 ors of protein kinase A such as forskolin or 3-isobutyl-1-methylxanthine.

13 nophosphate (cAMP) (forskolin (1-10 microM), 3-isobutyl-1-methylxanthine (0.1-1 mM), rolipram (10 mic

14 e of 1) phorbol myristic acid, forskolin and 3-isobutyl-1-methylxanthine, 2) BPDZ 154, or 3) 4-phenyl

15 ave similar IC(50) values for the inhibitors 3-isobutyl-1-methylxanthine (20 microM) and sildenafil (

16 combination of forskolin (20 micromol/L) and 3-isobutyl-1-methylxanthine (20 micromol/L), also inhibi

17 nselective phosphodiesterase (PDE) inhibitor 3-isobutyl-1-methylxanthine (20 mumol/L).

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

19 oromercuribenzene sulphonate (21 microM) and 3-isobutyl-1-methylxanthine (970 microM, partial inhibit

20 rst by dPGJ2 was enhanced in the presence of 3-isobutyl-1-methylxanthine, a cAMP phosphodiesterase in

21 In Leydig cells from wild-type mice, 3-isobutyl-1-methylxanthine, a compound that inhibits al

22 CF ASL; (ii). activating CFTR with forskolin/3-isobutyl-1-methylxanthine alkalinized NL ASL but acidi

23 3':5'-cyclic monophospate sodium), and IBMX (3-isobutyl-1-methylxanthine) also changed the splicing p

24 a2+ and blocked by 2',5'-dideoxyadenosine or 3-isobutyl-1-methylxanthine, an inhibitor of phosphodies

25 icroinjection of matched doses (300 nmol) of 3-isobutyl-1-methylxanthine and 7-deacetyl-7-O-(N-methyl

26 These effects were potentiated by 3-isobutyl-1-methylxanthine and attenuated by the adenyl

27 increases in intracellular cAMP prompted by 3-isobutyl-1-methylxanthine and forskolin partially mimi

28 However, 3-isobutyl-1-methylxanthine and forskolin treatment of a

29 n secretion (GSIS), and insulin secretion to 3-isobutyl-1-methylxanthine and KCl were all reduced wit

30 main in complex with non-selective inhibitor 3-isobutyl-1-methylxanthine and kinetic analysis on the

31 main (PDE5/6cd) complexed with sildenafil or 3-isobutyl-1-methylxanthine and the Pgamma-inhibitory pe

32 uld be prevented by dibutyryl cyclic-cAMP or 3-isobutyl-1-methylxanthine and the somatostatin (SST) r

33 Release was also stimulated by 3-isobutyl-1-methylxanthine and was additive with forsko

34 PDE6 with vardenafil or sildenafil (but not 3-isobutyl-1-methylxanthine and zaprinast) induced a dis

35 Forskolin, 3-isobutyl-1-methylxanthine, and 8-bromo-cAMP (8-Br-cAMP

36 of Tudor-SN (MEF-KO) impairs dexamethasone, 3-isobutyl-1-methylxanthine, and insulin (DMI)-induced a

37 s that increase [cAMP] (forskolin, rolipram, 3-isobutyl-1-methylxanthine, and papaverine) or mimic cA

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

39 uscles with the phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, and the adenylate cyclase a

40 on induced by 10 microm forskolin, 40 microm 3-isobutyl-1-methylxanthine caused a 50% reduction in my

41 AMP, or with the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine, caused a rightward shift in

42 gents known not to act on the cyclase, or by 3-isobutyl-1-methylxanthine, creatine phosphate, or crea

43 he increase in tyrosinase activity by either 3-isobutyl-1-methylxanthine, dibutyryl cAMP, or forskoli

44 ells by the combination of dexamethasone and 3-isobutyl-1-methylxanthine (DM) is suppressed by 2,3,7,

45 ic acid methyl ester hydrochloride (T-0156), 3-isobutyl-1-methylxanthine, EDTA, or cGMP, but not by c

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

47 100 nM forskolin, 1 mM 8-bromo-cAMP, or 1 mM 3-isobutyl-1-methylxanthine) had no effect on the amplit

48 2 in complex with the nonselective inhibitor 3-isobutyl-1-methylxanthine have been determined at medi

49 and its crystal structure as a complex with 3-isobutyl-1-methylxanthine (IBMX) at 1.55 A resolution.

50 The nonselective inhibitor 3-isobutyl-1-methylxanthine (IBMX) binds to a similar su

51 its crystal structures in the unliganded and 3-isobutyl-1-methylxanthine (IBMX) bound forms at 1.9 an

52 The phosphodiesterase (PDE) inhibitor 3-isobutyl-1-methylxanthine (IBMX) did not elevate cGMP

53 e continuously treated with forskolin and/or 3-isobutyl-1-methylxanthine (IBMX) in light-dark (LD) an

54 cose suppression and the increased effect of 3-isobutyl-1-methylxanthine (IBMX) observed in GADA+ don

55 3-Isobutyl-1-methylxanthine (IBMX) or 8-bromoadenosine 3

56 endogenous cAMP levels with either forskolin/3-isobutyl-1-methylxanthine (IBMX) or the V2 receptor ag

57 exposed to VIP, carbachol, forskolin, and/or 3-isobutyl-1-methylxanthine (IBMX) to determine whether

58 cGMP, vardenafil, sildenafil, tadalafil, or 3-isobutyl-1-methylxanthine (IBMX) were respectively wea

59 In the presence of 3-isobutyl-1-methylxanthine (IBMX), 10 microM SNC was su

60 3-Isobutyl-1-methylxanthine (IBMX), a non-specific phosp

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

62 l glucose and 10 mmol/l arginine, 0.1 mmol/l 3-isobutyl-1-methylxanthine (IBMX), and 5 micromol/l car

63 e of RINm5F cells to cAMP-increasing agents, 3-isobutyl-1-methylxanthine (IBMX), and forskolin comple

64 A nonselective PDE inhibitor, 3-isobutyl-1-methylxanthine (IBMX), and the PDE3 selecti

65 h or without the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), decreased the period

66 s exposed to the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), the circulating curr

67 MP was increased by the use of forskolin and 3-isobutyl-1-methylxanthine (IBMX), we show that increas

68 In transient transfections, forskolin plus 3-isobutyl-1-methylxanthine (IBMX), which increases intr

69 f the variants, leading to stable, forskolin+3-isobutyl-1-methylxanthine (IBMX)-activated whole-cell

70 nds with 5'-GMP, vardenafil, sildenafil, and 3-isobutyl-1-methylxanthine (IBMX).

71 (SNAP), and the phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (IBMX).

72 longed treatment with an adipogenic inducer, 3-isobutyl-1-methylxanthine (IBMX).

73 aintained in the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX).

74 llowing stimulation with forskolin (FSK) and 3-isobutyl-1-methylxanthine (IBMX).

75 presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX, 750 microM) reversibl

76 Incubating cells with PDGF and 3-isobutyl-1-methylxanthine (IBMX, a phosphodiesterase i

77 e competent in succinate-, ketoisocaproate-, 3-isobutyl-1-methylxanthine (IBMX-), KCl-, and tolbutami

78 cer, 10 micromol/L; >3-fold), potentiated by 3-isobutyl-1-methylxanthine (IBMX; phosphodiesterase typ

79 hosphodiesterase (cAMP-PDE) inhibitors, e.g. 3-isobutyl-1-methylxanthine [(IBMX) or caffeine, 10 mg/k

80 orskolin and the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine in proportion to increases i

81 presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine in the medium, suggesting ex

82 3-isobutyl-1-methylxanthine increased insulin secretion

83 nhibition of phosphodiesterase activity with 3-isobutyl-1-methylxanthine, indicating that alpha-adren

84 atment with the broad-spectrum PDE inhibitor 3-isobutyl-1-methylxanthine induced T cell CREB phosphor

85 ic PDE inhibitors for their ability to mimic 3-isobutyl-1-methylxanthine-induced ATF-1/CREB phosphory

86 The receptor inhibitor 3-isobutyl-1-methylxanthine inhibited the calcium respon

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

88 Following treatment with these diols or 3-isobutyl-1-methylxanthine, melanin and tyrosinase acti

89 or gamma (PPARgamma) by dexamethasone (DEX), 3-isobutyl-1-methylxanthine (MIX), and insulin.

90 treatment with forskolin, 8-bromo-cAMP, and 3-isobutyl-1-methylxanthine or by overexpression of the

91 3-Isobutyl-1-methylxanthine potentiated ATP-induced calc

92 of T cells with 8-bromo cAMP, forskolin, or 3-isobutyl-1-methylxanthine prevented the CD47-mediated

93 dependent protein kinase (PKA), MgATP, cGMP, 3-isobutyl-1-methylxanthine], shown earlier to produce S

94 l PDE5 constructs had similar affinities for 3-isobutyl-1-methylxanthine, sildenafil, tadalafil, and

95 The forskolin/3-isobutyl-1-methylxanthine-stimulated whole-cell conduc

96 vity, Km for cGMP, and IC50 for zaprinast or 3-isobutyl-1-methylxanthine were found among wild-type a

97 23187 or a combination of dibutyryl cAMP and 3-isobutyl-1-methylxanthine, which increase intracellula

98 3-isobutyl-1-methylxanthine, which potentiates the cGMP/

99 inhibitors, it is most potently inhibited by 3-isobutyl-1-methylxanthine with an IC(50) of 2.1 microM

100 imulating pGC by ANP/BNP, or blocking PDE by 3-isobutyl-1-methylxanthine/zaprinast caused significant