ライフサイエンスコーパス: isobutylmethylxanthine

1 n the absence of phosphodiesterase inhibitor isobutylmethylxanthine.

2 on of AMPK activity in response to forskolin/isobutylmethylxanthine.

3 d after G551D-CFTR activation with forskolin/isobutylmethylxanthine.

4 presence of the phosphodiesterase inhibitor isobutylmethylxanthine.

5 of cyclic nucleotide phosphodiesterase with isobutylmethylxanthine.

6 Dibutyryl cAMP (1 mM) plus isobutylmethylxanthine (0.25 mM) also enhanced alpha 1B-

7 that forskolin (1 microM) in the presence of isobutylmethylxanthine (0.25 mM) increased alpha 1B-AR n

8 d 7.6-fold, respectively) or to glucose plus isobutylmethylxanthine (10.8- and 15.1-fold, respectivel

9 was potentiated significantly by 100 pmol/l isobutylmethylxanthine (320%), 1 mmol/l oleate/palmitate

10 Both PDE1C enzymes were inhibited by isobutylmethylxanthine, 8-methoxymethyl isobutylmethylxa

11 Isobutylmethylxanthine and cholera toxin had the same ef

12 as well as extent to which up-regulation by isobutylmethylxanthine and cholera toxin was muted, was

13 oken cell preparations; and, that forskolin, isobutylmethylxanthine and isoproterenol elevate cyclic

14 etaTC3 cells is sensitive to 8-methoxymethyl isobutylmethylxanthine and zaprinast (IC(50) = 7.5 and 4

15 2 (FGF-2), in the presence of dexamethasone, isobutylmethylxanthine, and insulin, induces a prolonged

16 ipogenesis in the presence of dexamethasone, isobutylmethylxanthine, and insulin.

17 Forskolin, phosphodiesterase inhibitor isobutylmethylxanthine, and isoproterenol also significa

18 Forskolin, isobutylmethylxanthine, and the glucose-dependent insuli

19 The responses to forskolin plus isobutylmethylxanthine at neutral and acidic pH(o) were

20 muM of the phosphodiesterase (PDE) inhibitor isobutylmethylxanthine (by 33%).

21 nselective phosphodiesterase (PDE) inhibitor isobutylmethylxanthine, by PDE inhibitors selective for

22 orter, whereas forskolin, in the presence of isobutylmethylxanthine, decreased it.

23 Isobutylmethylxanthine-dependent activation of protein k

24 with the adipocyte differentiation mixture (isobutylmethylxanthine, dexamethasone, and insulin) or e

25 ted cells, and this effect is potentiated by isobutylmethylxanthine, dibutyryl-cAMP, or forskolin.

26 of 3T3-L1 adipocytes with isoproterenol and isobutylmethylxanthine disperses CGI-58 from the surface

27 nently expressing human TSHRs incubated with isobutylmethylxanthine for 30 min after washing the cell

28 Forskolin, 8-bromo cAMP, and isobutylmethylxanthine (IBMX) all prevented CD47-mediate

29 ence of the cAMP phosphodiesterase inhibitor isobutylmethylxanthine (IBMX) or the cell permeant cAMP

30 treatment with adenosine receptor antagonist isobutylmethylxanthine (IBMX) or with adenosine uptake i

31 n incubation of the cells with forskolin and isobutylmethylxanthine (IBMX) to elevate levels of cAMP

32 nergize with the phosphodiesterase inhibitor isobutylmethylxanthine (IBMX) to promote cell death in 3

33 We previously reported that isobutylmethylxanthine (IBMX), a derivative of oxypurine

34 Incubation of 3T3-L1 preadipocytes with isobutylmethylxanthine (IBMX), dexamethasone, and insuli

35 ated that the phosphodiesterase inhibitor, 3-isobutylmethylxanthine (IBMX), inhibited urea synthesis

36 vity with a broad-spectrum PDE inhibitor, 3'-isobutylmethylxanthine (IBMX), produced a 9-fold increas

37 ctivation of DeltaF508-CFTR by forskolin and isobutylmethylxanthine (IBMX).

38 levels using the phosphodiesterase inhibitor isobutylmethylxanthine (IBMX; 10 microM), the non-hydrol

39 taste buds with forskolin (Fsk; 1 microm) + isobutylmethylxanthine (IBMX; 100 microm), which elevate

40 of differentiation; insulin, dexamethasone, isobutylmethylxanthine (IDX), or IDX plus trichostatin A

41 two-electrode voltage-clamp, forskolin plus isobutylmethylxanthine induced a Ca(2+)-dependent increa

42 e to exposure of the cells to dexamethasone, isobutylmethylxanthine, insulin, and a PPARgamma ligand.

43 that induces adipocyte differentiation, i.e. isobutylmethylxanthine, insulin, and dexamethasone.

44 n response to induction by dexamethasone and isobutylmethylxanthine is blocked by inhibitors of Ca2+-

45 pocytes to insulin, dexamethasone (DEX), and isobutylmethylxanthine (MIX) leads to the phosphorylatio

46 t-confluent 3T3-L1 preadipocytes to insulin, isobutylmethylxanthine (MIX), dexamethasone (DEX), and f

47 Elevation of intracellular cAMP levels with isobutylmethylxanthine or forskolin had no effect on AMP

48 GMP was measured in the presence of 10(-3) M isobutylmethylxanthine or Zaprinast, two different inhib

49 at treatment with forskolin, dibutyryl cAMP, isobutylmethylxanthine, or isoproterenol activate cellul

50 8-bromo-cGMP, or phosphodiesterase inhibitor isobutylmethylxanthine to mimic the increased Ca(2+) inf

51 Pretreatment with forskolin or isobutylmethylxanthine to stimulate cAMP did not affect

52 ducing agents (isoproterenol, forskolin, and isobutylmethylxanthine), which stimulate lipolysis and a

53 erved following treatment with forskolin and isobutylmethylxanthine, which decreases fibroblast migra

54 d by isobutylmethylxanthine, 8-methoxymethyl isobutylmethylxanthine, zaprinast, and vinpocetine.