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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 tion cocktail of dexamethasone, insulin, and isobutylmethylxanthine alone or the cocktail plus glucos
12                                              Isobutylmethylxanthine and cholera toxin had the same ef
13  as well as extent to which up-regulation by isobutylmethylxanthine and cholera toxin was muted, was
14 oken cell preparations; and, that forskolin, isobutylmethylxanthine and isoproterenol elevate cyclic
15 etaTC3 cells is sensitive to 8-methoxymethyl isobutylmethylxanthine and zaprinast (IC(50) = 7.5 and 4
16 2 (FGF-2), in the presence of dexamethasone, isobutylmethylxanthine, and insulin, induces a prolonged
17 ipogenesis in the presence of dexamethasone, isobutylmethylxanthine, and insulin.
18       Forskolin, phosphodiesterase inhibitor isobutylmethylxanthine, and isoproterenol also significa
19                                   Forskolin, isobutylmethylxanthine, and the glucose-dependent insuli
20              The responses to forskolin plus isobutylmethylxanthine at neutral and acidic pH(o) were
21 muM of the phosphodiesterase (PDE) inhibitor isobutylmethylxanthine (by 33%).
22 nselective phosphodiesterase (PDE) inhibitor isobutylmethylxanthine, by PDE inhibitors selective for
23 orter, whereas forskolin, in the presence of isobutylmethylxanthine, decreased it.
24                                              Isobutylmethylxanthine-dependent activation of protein k
25  with the adipocyte differentiation mixture (isobutylmethylxanthine, dexamethasone, and insulin) or e
26 ted cells, and this effect is potentiated by isobutylmethylxanthine, dibutyryl-cAMP, or forskolin.
27  of 3T3-L1 adipocytes with isoproterenol and isobutylmethylxanthine disperses CGI-58 from the surface
28 nently expressing human TSHRs incubated with isobutylmethylxanthine for 30 min after washing the cell
29                 Forskolin, 8-bromo cAMP, and isobutylmethylxanthine (IBMX) all prevented CD47-mediate
30 ence of the cAMP phosphodiesterase inhibitor isobutylmethylxanthine (IBMX) or the cell permeant cAMP
31 treatment with adenosine receptor antagonist isobutylmethylxanthine (IBMX) or with adenosine uptake i
32 n incubation of the cells with forskolin and isobutylmethylxanthine (IBMX) to elevate levels of cAMP
33 nergize with the phosphodiesterase inhibitor isobutylmethylxanthine (IBMX) to promote cell death in 3
34                  We previously reported that isobutylmethylxanthine (IBMX), a derivative of oxypurine
35      Incubation of 3T3-L1 preadipocytes with isobutylmethylxanthine (IBMX), dexamethasone, and insuli
36 ated that the phosphodiesterase inhibitor, 3-isobutylmethylxanthine (IBMX), inhibited urea synthesis
37 vity with a broad-spectrum PDE inhibitor, 3'-isobutylmethylxanthine (IBMX), produced a 9-fold increas
38 ctivation of DeltaF508-CFTR by forskolin and isobutylmethylxanthine (IBMX).
39 levels using the phosphodiesterase inhibitor isobutylmethylxanthine (IBMX; 10 microM), the non-hydrol
40  taste buds with forskolin (Fsk; 1 microm) + isobutylmethylxanthine (IBMX; 100 microm), which elevate
41  of differentiation; insulin, dexamethasone, isobutylmethylxanthine (IDX), or IDX plus trichostatin A
42  two-electrode voltage-clamp, forskolin plus isobutylmethylxanthine induced a Ca(2+)-dependent increa
43 e to exposure of the cells to dexamethasone, isobutylmethylxanthine, insulin, and a PPARgamma ligand.
44 that induces adipocyte differentiation, i.e. isobutylmethylxanthine, insulin, and dexamethasone.
45 n response to induction by dexamethasone and isobutylmethylxanthine is blocked by inhibitors of Ca2+-
46 pocytes to insulin, dexamethasone (DEX), and isobutylmethylxanthine (MIX) leads to the phosphorylatio
47 t-confluent 3T3-L1 preadipocytes to insulin, isobutylmethylxanthine (MIX), dexamethasone (DEX), and f
48  Elevation of intracellular cAMP levels with isobutylmethylxanthine or forskolin had no effect on AMP
49 GMP was measured in the presence of 10(-3) M isobutylmethylxanthine or Zaprinast, two different inhib
50 at treatment with forskolin, dibutyryl cAMP, isobutylmethylxanthine, or isoproterenol activate cellul
51 8-bromo-cGMP, or phosphodiesterase inhibitor isobutylmethylxanthine to mimic the increased Ca(2+) inf
52               Pretreatment with forskolin or isobutylmethylxanthine to stimulate cAMP did not affect
53 ducing agents (isoproterenol, forskolin, and isobutylmethylxanthine), which stimulate lipolysis and a
54 erved following treatment with forskolin and isobutylmethylxanthine, which decreases fibroblast migra
55 d by isobutylmethylxanthine, 8-methoxymethyl isobutylmethylxanthine, zaprinast, and vinpocetine.