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In addition, << ethanol >> induced degradation of DNA methyltransferases (DNMT-1, DNMT-3a, and DNMT-3b), as well as the methyl CpG-binding proteins ([[ MeCP-2 ]], MBD-2 and MBD-3), in MEF cells by the proteasomal pathway.

In addition, << ethanol >> induced degradation of DNA methyltransferases (DNMT-1, DNMT-3a, and DNMT-3b), as well as the methyl CpG-binding proteins (MeCP-2, [[ MBD-2 ]] and MBD-3), in MEF cells by the proteasomal pathway.

In addition, << ethanol >> induced degradation of DNA methyltransferases (DNMT-1, DNMT-3a, and DNMT-3b), as well as the methyl CpG-binding proteins (MeCP-2, MBD-2 and [[ MBD-3 ]]), in MEF cells by the proteasomal pathway.

Comparison of the << monoamine oxidase >> inhibiting properties of two reversible and selective monoamine oxidase-A inhibitors [[ moclobemide ]] and toloxatone, and assessment of their effect on psychometric performance in healthy subjects.

Comparison of the monoamine oxidase inhibiting properties of two reversible and selective << monoamine oxidase-A >> inhibitors [[ moclobemide ]] and toloxatone, and assessment of their effect on psychometric performance in healthy subjects.

Comparison of the << monoamine oxidase >> inhibiting properties of two reversible and selective monoamine oxidase-A inhibitors moclobemide and [[ toloxatone ]], and assessment of their effect on psychometric performance in healthy subjects.

Comparison of the monoamine oxidase inhibiting properties of two reversible and selective << monoamine oxidase-A >> inhibitors moclobemide and [[ toloxatone ]], and assessment of their effect on psychometric performance in healthy subjects.

The effects of two reversible, predominantly << monoamine oxidase-A >> (MAO-A) inhibitors, [[ moclobemide ]] (150 mg three times daily) and toloxatone (400-200-400 mg day-1) on monoamine metabolites and psychometric performance were compared in a double-blind placebo controlled crossover study in 12 healthy subjects.

The effects of two reversible, predominantly << monoamine oxidase-A >> (MAO-A) inhibitors, moclobemide (150 mg three times daily) and [[ toloxatone ]] (400-200-400 mg day-1) on monoamine metabolites and psychometric performance were compared in a double-blind placebo controlled crossover study in 12 healthy subjects.

Before the next drug intake, << MAO-A >> inhibition, as judged by the decrease of plasma DHPG concentration, was significantly different from placebo with [[ moclobemide ]] but not with toloxatone.

Before the next drug intake, << MAO-A >> inhibition, as judged by the decrease of plasma DHPG concentration, was significantly different from placebo with moclobemide but not with [[ toloxatone ]].

Previously, we have found that << BRN-103 >>, a nicotinamide derivative, inhibits vascular endothelial growth factor ([[ VEGF ]])-mediated angiogenesis signaling in human endothelial cells.

Previously, we have found that << BRN-103 >>, a nicotinamide derivative, inhibits [[ vascular endothelial growth factor ]] (VEGF)-mediated angiogenesis signaling in human endothelial cells.

Previously, we have found that BRN-103, a << nicotinamide >> derivative, inhibits vascular endothelial growth factor ([[ VEGF ]])-mediated angiogenesis signaling in human endothelial cells.

Previously, we have found that BRN-103, a << nicotinamide >> derivative, inhibits [[ vascular endothelial growth factor ]] (VEGF)-mediated angiogenesis signaling in human endothelial cells.

Furthermore, << BRN-250 >> inhibited the [[ VEGF ]]-induced phosphorylation and intracellular tyrosine kinase activity of VEGF receptor 2 (VEGFR2) and the activation of its downstream AKT pathway.

Furthermore, << BRN-250 >> inhibited the VEGF-induced phosphorylation and intracellular [[ tyrosine kinase ]] activity of VEGF receptor 2 (VEGFR2) and the activation of its downstream AKT pathway.

Furthermore, << BRN-250 >> inhibited the VEGF-induced phosphorylation and intracellular tyrosine kinase activity of [[ VEGF receptor 2 ]] (VEGFR2) and the activation of its downstream AKT pathway.

Furthermore, << BRN-250 >> inhibited the VEGF-induced phosphorylation and intracellular tyrosine kinase activity of VEGF receptor 2 ([[ VEGFR2 ]]) and the activation of its downstream AKT pathway.

Furthermore, << BRN-250 >> inhibited the VEGF-induced phosphorylation and intracellular tyrosine kinase activity of VEGF receptor 2 (VEGFR2) and the activation of its downstream [[ AKT ]] pathway.

Inhibition of << gelatinase A >> (MMP-2) by [[ batimastat ]] and captopril reduces tumor growth and lung metastases in mice bearing Lewis lung carcinoma.

Inhibition of gelatinase A (<< MMP-2 >>) by [[ batimastat ]] and captopril reduces tumor growth and lung metastases in mice bearing Lewis lung carcinoma.

Inhibition of << gelatinase A >> (MMP-2) by batimastat and [[ captopril ]] reduces tumor growth and lung metastases in mice bearing Lewis lung carcinoma.

Inhibition of gelatinase A (<< MMP-2 >>) by batimastat and [[ captopril ]] reduces tumor growth and lung metastases in mice bearing Lewis lung carcinoma.

We have examined the effects of the synthetic << matrix metalloproteinase >> inhibitor, [[ batimastat ]] (BB-94) and the angiotensin-converting enzyme inhibitor, captopril, on metalloproteinase activity of murine Lewis-lung-carcinoma cells (3LL) in vitro, and on local growth and lung metastasis of the same tumor implanted intramuscularly in syngeneic C57BL/6 mice.

We have examined the effects of the synthetic << matrix metalloproteinase >> inhibitor, batimastat ([[ BB-94 ]]) and the angiotensin-converting enzyme inhibitor, captopril, on metalloproteinase activity of murine Lewis-lung-carcinoma cells (3LL) in vitro, and on local growth and lung metastasis of the same tumor implanted intramuscularly in syngeneic C57BL/6 mice.

We have examined the effects of the synthetic matrix metalloproteinase inhibitor, batimastat (BB-94) and the << angiotensin-converting enzyme >> inhibitor, [[ captopril ]], on metalloproteinase activity of murine Lewis-lung-carcinoma cells (3LL) in vitro, and on local growth and lung metastasis of the same tumor implanted intramuscularly in syngeneic C57BL/6 mice.

Here we report that << captopril >> treatment resulted in decreased transcription and protein levels of [[ gelatinase A ]] by 3LL cells.

Both << BB-94 >> and captopril also prevented substrate degradation by [[ gelatinase A and B ]] released in conditioned medium by cultured cells.

Methionine synthase reductase (<< MTRR >>) is an enzyme involved in the conversion of Hcy to [[ methionine ]].

<< Methionine synthase reductase >> (MTRR) is an enzyme involved in the conversion of Hcy to [[ methionine ]].

Methionine synthase reductase (<< MTRR >>) is an enzyme involved in the conversion of [[ Hcy ]] to methionine.

<< Methionine synthase reductase >> (MTRR) is an enzyme involved in the conversion of [[ Hcy ]] to methionine.

<< GPxs >> reduce hydroperoxides to the corresponding [[ alcohols ]] by means of glutathione (GSH).

<< TCDD >> decreased the expression of the [[ glucose transporter ]], SLC2A1, and most of the glycolytic transcripts, followed by decreases in glycolytic intermediates, including pyruvate.

<< TCDD >> decreased the expression of the glucose transporter, [[ SLC2A1 ]], and most of the glycolytic transcripts, followed by decreases in glycolytic intermediates, including pyruvate.

Mitochondrial << glutathione (GSH) reductase >> activity and the GSH/glutathione disulfide ratio were decreased by [[ TCDD ]], ultimately leading to mitochondrial dysfunction, characterized by decreased inner mitochondrial membrane potential and ATP production, and increased production of the reactive oxygen species (ROS), hydrogen peroxide.

<< ATP-binding cassette transporter A1 >> is involved in hepatic [[ alpha-tocopherol ]] secretion.

alpha-Tocopherol transfer protein (<< alpha-TTP >>), the product of the gene responsible for familial isolated vitamin E deficiency, plays an important role in maintaining the plasma [[ alpha-tocopherol ]] level by mediating the secretion of alpha-tocopherol by the liver.

<< alpha-Tocopherol transfer protein >> (alpha-TTP), the product of the gene responsible for familial isolated vitamin E deficiency, plays an important role in maintaining the plasma [[ alpha-tocopherol ]] level by mediating the secretion of alpha-tocopherol by the liver.

alpha-Tocopherol transfer protein (<< alpha-TTP >>), the product of the gene responsible for familial isolated vitamin E deficiency, plays an important role in maintaining the plasma alpha-tocopherol level by mediating the secretion of [[ alpha-tocopherol ]] by the liver.

<< alpha-Tocopherol transfer protein >> (alpha-TTP), the product of the gene responsible for familial isolated vitamin E deficiency, plays an important role in maintaining the plasma alpha-tocopherol level by mediating the secretion of [[ alpha-tocopherol ]] by the liver.

First, addition of << apolipoprotein A-I >> (apoA-I), a direct acceptor of the ATP-binding cassette transporter A1 (ABCA1)-secreted lipids, increased [[ alpha-tocopherol ]] secretion in a dose-dependent manner.

First, addition of apolipoprotein A-I (<< apoA-I >>), a direct acceptor of the ATP-binding cassette transporter A1 (ABCA1)-secreted lipids, increased [[ alpha-tocopherol ]] secretion in a dose-dependent manner.

First, addition of apolipoprotein A-I (apoA-I), a direct acceptor of the << ATP-binding cassette transporter A1 >> (ABCA1)-secreted lipids, increased [[ alpha-tocopherol ]] secretion in a dose-dependent manner.

First, addition of apolipoprotein A-I (apoA-I), a direct acceptor of the ATP-binding cassette transporter A1 (<< ABCA1 >>)-secreted lipids, increased [[ alpha-tocopherol ]] secretion in a dose-dependent manner.

Second, << probucol >>, an antiatherogenic compound reported to be an inactivator of [[ ABCA1 ]] reduced hepatic alpha-tocopherol secretion.

Third, << ABCA1 >>-RNAi suppressed hepatic [[ alpha-tocopherol ]] secretion.

These results strongly suggest that << ABCA1 >> is substantially involved in hepatic [[ alpha-tocopherol ]] secretion.

<< 2-Amino-3-[3-hydroxy-5-(2-thiazolyl)-4-isoxazolyl]propionic acid >> (1) is a potent [[ AMPA receptor ]] agonist with moderate affinity for native kainic acid (KA) receptors, whereas (S)-E-4-(2,2-dimethylpropylidene)glutamic acid (3) show high affinity for the GluR5 subtype of KA receptors and much lower affinity for the GluR2 subtype of AMPA receptors.

<< Pranlukast >>, a leukotriene receptor antagonist, inhibits [[ interleukin-5 ]] production via a mechanism distinct from leukotriene receptor antagonism.

<< Pranlukast >>, a leukotriene receptor antagonist, inhibits interleukin-5 production via a mechanism distinct from [[ leukotriene receptor ]] antagonism.

<< Pranlukast >>, a [[ leukotriene receptor ]] antagonist, inhibits interleukin-5 production via a mechanism distinct from leukotriene receptor antagonism.

BACKGROUND: << Pranlukast >>, a [[ cysteinyl leukotriene receptor 1 ]] (CysLTR1) antagonist, inhibits not only airway smooth muscle contraction, but also allergic inflammation.

BACKGROUND: << Pranlukast >>, a cysteinyl leukotriene receptor 1 ([[ CysLTR1 ]]) antagonist, inhibits not only airway smooth muscle contraction, but also allergic inflammation.

The aim of this study was to determine the mechanism of << pranlukast >>-induced [[ interleukin-5 ]] (IL-5) inhibition in allergic inflammation.

The aim of this study was to determine the mechanism of << pranlukast >>-induced interleukin-5 ([[ IL-5 ]]) inhibition in allergic inflammation.

RESULTS: Pretreatment of lung tissues with << pranlukast >> alone significantly decreased the amount of [[ IL-5 ]] protein in the culture medium by 40%.

<< Pranlukast >>-induced inhibition of [[ IL-5 ]] mRNA expression was noted in various cells, irrespective of their CysLTR1 mRNA expression status.

CONCLUSION: Our results indicate that << pranlukast >> inhibits [[ IL-5 ]] synthesis via a mechanism distinct from CysLTR1 antagonism.

CONCLUSION: Our results indicate that << pranlukast >> inhibits IL-5 synthesis via a mechanism distinct from [[ CysLTR1 ]] antagonism.

<< Thiazolidinediones >> are a new class of anti-diabetic agents which increase insulin sensitivity by binding to the peroxisome proliferator-activated receptor gamma (PPAR(gamma)) and stimulating the expression of [[ insulin ]]-responsive genes involved in glucose and lipid metabolism.

<< Thiazolidinediones >> are a new class of anti-diabetic agents which increase [[ insulin ]] sensitivity by binding to the peroxisome proliferator-activated receptor gamma (PPAR(gamma)) and stimulating the expression of insulin-responsive genes involved in glucose and lipid metabolism.

The effect of troglitazone on ENT1 was PPAR(gamma)-independent and kinetic studies revealed that << troglitazone >> was a competitive inhibitor of [[ ENT1 ]].

The difference in structure of << troglitazone >> did not account for its inhibitory effect on [[ ENT1 ]] because Vitamin E did not inhibit [3H]adenosine uptake by HASMCs.

Using the nucleoside transporter deficient PK15NTD cells stably expressing ENT1 and ENT2, it was found that << troglitazone >> inhibited [[ ENT1 ]] but had no effect on ENT2.

From these results, it is suggested that << troglitazone >> may enhance the vasodilatory effect of adenosine by inhibiting [[ ENT1 ]].

Pharmacologically, << troglitazone >> is a novel inhibitor of [[ ENT1 ]].

<< Phenytoin >> is principally metabolized by [[ CYP2C9 ]], and both are probable substrates of the drug transporter P-glycoprotein.

<< Phenytoin >> is principally metabolized by CYP2C9, and both are probable substrates of the [[ drug transporter ]] P-glycoprotein.

<< Phenytoin >> is principally metabolized by CYP2C9, and both are probable substrates of the drug transporter [[ P-glycoprotein ]].

<< Fisetin >> treatment of preadipocytes reduced the phosphorylation of [[ S6K1 ]] and mTORC1 in a time- and concentration-dependent manner.

<< Fisetin >> treatment of preadipocytes reduced the phosphorylation of S6K1 and [[ mTORC1 ]] in a time- and concentration-dependent manner.

To further our understanding of how << fisetin >> negatively regulates [[ mTORC1 ]] signaling, we analyzed the phosphorylation of S6K1, mTOR and Akt in fisetin-treated TSC2-knockdown cells.

The results suggested that << fisetin >> treatment inhibits [[ mTORC1 ]] activity in an Akt-dependent manner.

The results suggested that << fisetin >> treatment inhibits mTORC1 activity in an [[ Akt ]]-dependent manner.

Fisetin treatment inhibited adipocyte differentiation, consistent with the negative effect of << fisetin >> on [[ mTOR ]].

We also observed that << fisetin >> efficiently suppressed the phosphorylation of [[ Akt ]], S6K1 and mTORC1 in adipose tissue.

We also observed that << fisetin >> efficiently suppressed the phosphorylation of Akt, [[ S6K1 ]] and mTORC1 in adipose tissue.

We also observed that << fisetin >> efficiently suppressed the phosphorylation of Akt, S6K1 and [[ mTORC1 ]] in adipose tissue.

Collectively, these results suggest that inhibition of << mTORC1 >> signaling by [[ fisetin ]] prevents adipocyte differentiation of 3T3-L1 preadipocytes and obesity in HFD-fed mice.

Cyclin E-cdk2 activation is associated with cell cycle arrest and inhibition of DNA replication induced by the << thymidylate synthase >> inhibitor [[ Tomudex ]].

<< Tomudex >> (ZD1694) is a specific antifolate-based [[ thymidylate synthase ]] inhibitor active in a variety of solid tumor malignancies.

Studies were carried out in vitro to evaluate downstream molecular alterations induced as a consequence of the potent and sustained inhibition of << thymidylate synthase >> by [[ Tomudex ]].

<< Tomudex >> treatment resulted in the decrease in p27(kip1) expression, with an increase in cyclin E and cdk2 protein expression and [[ kinase ]] activities 24 h after a 2-h exposure.

<< Tomudex >> treatment resulted in the decrease in p27(kip1) expression, with an increase in [[ cyclin E ]] and cdk2 protein expression and kinase activities 24 h after a 2-h exposure.

<< Tomudex >> treatment resulted in the decrease in p27(kip1) expression, with an increase in cyclin E and [[ cdk2 ]] protein expression and kinase activities 24 h after a 2-h exposure.

<< Tomudex >> treatment resulted in the decrease in [[ p27(kip1) ]] expression, with an increase in cyclin E and cdk2 protein expression and kinase activities 24 h after a 2-h exposure.

The studies with dThyd rescue from << cyclin E >>-cdk2 protein overexpression and growth inhibition by [[ Tomudex ]] indicate that increased cyclin E-cdk2 protein expression is associated with effective inhibition of thymidylate synthase and resultant dNTP pool imbalance.

The studies with dThyd rescue from cyclin E-<< cdk2 >> protein overexpression and growth inhibition by [[ Tomudex ]] indicate that increased cyclin E-cdk2 protein expression is associated with effective inhibition of thymidylate synthase and resultant dNTP pool imbalance.

The studies with dThyd rescue from cyclin E-cdk2 protein overexpression and growth inhibition by << Tomudex >> indicate that increased [[ cyclin E ]]-cdk2 protein expression is associated with effective inhibition of thymidylate synthase and resultant dNTP pool imbalance.

The studies with dThyd rescue from cyclin E-cdk2 protein overexpression and growth inhibition by << Tomudex >> indicate that increased cyclin E-[[ cdk2 ]] protein expression is associated with effective inhibition of thymidylate synthase and resultant dNTP pool imbalance.

The studies with dThyd rescue from << cyclin E >>-cdk2 protein overexpression and growth inhibition by [[ Tomudex ]] indicate that increased cyclin E-cdk2 protein expression is associated with effective inhibition of thymidylate synthase and resultant dNTP pool imbalance.

The studies with dThyd rescue from cyclin E-<< cdk2 >> protein overexpression and growth inhibition by [[ Tomudex ]] indicate that increased cyclin E-cdk2 protein expression is associated with effective inhibition of thymidylate synthase and resultant dNTP pool imbalance.

The studies with dThyd rescue from cyclin E-cdk2 protein overexpression and growth inhibition by << Tomudex >> indicate that increased cyclin E-cdk2 protein expression is associated with effective inhibition of [[ thymidylate synthase ]] and resultant dNTP pool imbalance.

These results suggest that the megabase DNA fragmentation is induced as a consequence of inhibition of thymidylate synthase by << Tomudex >> and kilobase DNA fragmentation may correlate with the reduction of p27(kip1) expression and the increase in [[ cyclin E ]] and cdk2 kinase activities.

These results suggest that the megabase DNA fragmentation is induced as a consequence of inhibition of thymidylate synthase by << Tomudex >> and kilobase DNA fragmentation may correlate with the reduction of p27(kip1) expression and the increase in cyclin E and [[ cdk2 ]] kinase activities.

These results suggest that the megabase DNA fragmentation is induced as a consequence of inhibition of thymidylate synthase by << Tomudex >> and kilobase DNA fragmentation may correlate with the reduction of p27(kip1) expression and the increase in cyclin E and cdk2 [[ kinase ]] activities.

These results suggest that the megabase DNA fragmentation is induced as a consequence of inhibition of thymidylate synthase by << Tomudex >> and kilobase DNA fragmentation may correlate with the reduction of [[ p27(kip1) ]] expression and the increase in cyclin E and cdk2 kinase activities.

These results suggest that the megabase DNA fragmentation is induced as a consequence of inhibition of << thymidylate synthase >> by [[ Tomudex ]] and kilobase DNA fragmentation may correlate with the reduction of p27(kip1) expression and the increase in cyclin E and cdk2 kinase activities.