The potency of the selective alpha 1D-adrenoceptor antagonist BMY 7378 against noradrenaline (pA2 = 6.16 +/- 0.13) and of the selective << alpha 1A-adrenoceptor >> antagonist [[ RS-17053 ]] against noradrenaline (pKB = 8.35 +/- 0.10) and against the selective alpha 1A-adrenoceptor agonist A-61603 (pKB = 8.40 +/- 0.09) were too low to account for alpha 1D- and alpha 1A-adrenoceptor involvement.


Doses of dimethocaine (1.7 mg/kg) and cocaine (0.3 mg/kg) which produced full (> 80%) substitution for cocaine were administered in combination with the << dopamine D1 receptor >> antagonist [[ SCH 39166 ]] ((-)-trans-6,7,7a,8,9,13b-hexahydro-3-chloro-2-hydroxy-N-methyl-5H -benzo [d]naphtho-(2,1-b)azepine) and the dopamine D2 receptor antagonist raclopride (both at 0.003-0.03 mg/kg).


Doses of dimethocaine (1.7 mg/kg) and cocaine (0.3 mg/kg) which produced full (> 80%) substitution for cocaine were administered in combination with the << dopamine D1 receptor >> antagonist SCH 39166 ([[ (-)-trans-6,7,7a,8,9,13b-hexahydro-3-chloro-2-hydroxy-N-methyl-5H -benzo [d]naphtho-(2,1-b)azepine ]]) and the dopamine D2 receptor antagonist raclopride (both at 0.003-0.03 mg/kg).


Doses of dimethocaine (1.7 mg/kg) and cocaine (0.3 mg/kg) which produced full (> 80%) substitution for cocaine were administered in combination with the dopamine D1 receptor antagonist SCH 39166 ((-)-trans-6,7,7a,8,9,13b-hexahydro-3-chloro-2-hydroxy-N-methyl-5H -benzo [d]naphtho-(2,1-b)azepine) and the << dopamine D2 receptor >> antagonist [[ raclopride ]] (both at 0.003-0.03 mg/kg).


<< Carvedilol >> reduced the risk of death or heart failure in patients with above-median levels of [[ N-BNP ]] or adrenomedullin, or both, to rates not significantly different from those observed in patients with levels below the median value.


<< Carvedilol >> reduced the risk of death or heart failure in patients with above-median levels of N-BNP or [[ adrenomedullin ]], or both, to rates not significantly different from those observed in patients with levels below the median value.


<< Carvedilol >> reduced mortality and heart failure in patients with higher pre-treatment plasma [[ N-BNP ]] and adrenomedullin.


<< Carvedilol >> reduced mortality and heart failure in patients with higher pre-treatment plasma N-BNP and [[ adrenomedullin ]].


In combination with << clofarabine >>, the ability of resveratrol to reduce the contents of [[ Sp1 ]] and its target gene products was also evident in a time- and dose-dependent experiment.


In combination with clofarabine, the ability of << resveratrol >> to reduce the contents of [[ Sp1 ]] and its target gene products was also evident in a time- and dose-dependent experiment.


The inhibition of phosphoinositide 3-kinase using << Ly294002 >> augmented a decrease in the [[ p21 ]] level induced by their combination, but it showed no significant effects on expression of Sp1 and cyclin D1.


The inhibition of << phosphoinositide 3-kinase >> using [[ Ly294002 ]] augmented a decrease in the p21 level induced by their combination, but it showed no significant effects on expression of Sp1 and cyclin D1.


Taken together, the data provide evidence that the synergistic antiproliferative effect of << resveratrol >> and clofarabine is linked to the inhibition of [[ Akt ]] and Sp1 activities, and suggest that this combination may have therapeutic value in treatment of malignant mesothelioma.


Taken together, the data provide evidence that the synergistic antiproliferative effect of << resveratrol >> and clofarabine is linked to the inhibition of Akt and [[ Sp1 ]] activities, and suggest that this combination may have therapeutic value in treatment of malignant mesothelioma.


Taken together, the data provide evidence that the synergistic antiproliferative effect of resveratrol and << clofarabine >> is linked to the inhibition of [[ Akt ]] and Sp1 activities, and suggest that this combination may have therapeutic value in treatment of malignant mesothelioma.


Taken together, the data provide evidence that the synergistic antiproliferative effect of resveratrol and << clofarabine >> is linked to the inhibition of Akt and [[ Sp1 ]] activities, and suggest that this combination may have therapeutic value in treatment of malignant mesothelioma.


<< Phillyrin >> attenuates high glucose-induced lipid accumulation in human HepG2 hepatocytes through the activation of [[ LKB1 ]]/AMP-activated protein kinase-dependent signalling.


<< Phillyrin >> attenuates high glucose-induced lipid accumulation in human HepG2 hepatocytes through the activation of LKB1/[[ AMP-activated protein kinase ]]-dependent signalling.


Phillyrin strongly inhibited high << glucose >>-induced [[ fatty acid synthase ]] (FAS) expression by modulating sterol regulatory element-binding protein-1c (SREBP-1c) activation.


Phillyrin strongly inhibited high << glucose >>-induced fatty acid synthase ([[ FAS ]]) expression by modulating sterol regulatory element-binding protein-1c (SREBP-1c) activation.


<< Phillyrin >> strongly inhibited high glucose-induced [[ fatty acid synthase ]] (FAS) expression by modulating sterol regulatory element-binding protein-1c (SREBP-1c) activation.


<< Phillyrin >> strongly inhibited high glucose-induced fatty acid synthase ([[ FAS ]]) expression by modulating sterol regulatory element-binding protein-1c (SREBP-1c) activation.


Moreover, use of the pharmacological << AMP-activated protein kinase >> (AMPK) inhibitor [[ compound C ]] revealed that AMPK is essential for suppressing SREBP-1c expression in phillyrin-treated cells.


Moreover, use of the pharmacological AMP-activated protein kinase (<< AMPK >>) inhibitor [[ compound C ]] revealed that AMPK is essential for suppressing SREBP-1c expression in phillyrin-treated cells.


Moreover, use of the pharmacological AMP-activated protein kinase (AMPK) inhibitor << compound C >> revealed that [[ AMPK ]] is essential for suppressing SREBP-1c expression in phillyrin-treated cells.


Finally, we found that liver kinase B1 (LKB1) phosphorylation is required for the << phillyrin >>-enhanced activation of [[ AMPK ]] in HepG2 hepatocytes.


These results indicate that << phillyrin >> prevents lipid accumulation in HepG2 cells by blocking the expression of SREBP-1c and FAS through [[ LKB1 ]]/AMPK activation, suggesting that phillyrin is a novel AMPK activator with a role in the prevention and treatment of obesity.


These results indicate that << phillyrin >> prevents lipid accumulation in HepG2 cells by blocking the expression of SREBP-1c and FAS through LKB1/[[ AMPK ]] activation, suggesting that phillyrin is a novel AMPK activator with a role in the prevention and treatment of obesity.


These results indicate that phillyrin prevents lipid accumulation in HepG2 cells by blocking the expression of SREBP-1c and FAS through LKB1/AMPK activation, suggesting that << phillyrin >> is a novel [[ AMPK ]] activator with a role in the prevention and treatment of obesity.


These results indicate that << phillyrin >> prevents lipid accumulation in HepG2 cells by blocking the expression of [[ SREBP-1c ]] and FAS through LKB1/AMPK activation, suggesting that phillyrin is a novel AMPK activator with a role in the prevention and treatment of obesity.


These results indicate that << phillyrin >> prevents lipid accumulation in HepG2 cells by blocking the expression of SREBP-1c and [[ FAS ]] through LKB1/AMPK activation, suggesting that phillyrin is a novel AMPK activator with a role in the prevention and treatment of obesity.


<< Benzenesulfonamides >> incorporating cyanoacrylamide moieties strongly inhibit [[ Saccharomyces cerevisiae β-carbonic anhydrase ]].


Benzenesulfonamides incorporating << cyanoacrylamide >> moieties strongly inhibit [[ Saccharomyces cerevisiae β-carbonic anhydrase ]].


A series of << benzenesulfonamides >> incorporating cyanoacrylamide moieties (tyrphostine analogs) were assayed as inhibitors of the β-carbonic anhydrase (CA, [[ EC 4.2.1.1 ]]) from Saccharomyces cerevisiae, ScCA.


A series of << benzenesulfonamides >> incorporating cyanoacrylamide moieties (tyrphostine analogs) were assayed as inhibitors of the β-carbonic anhydrase (CA, EC 4.2.1.1) from Saccharomyces cerevisiae, [[ ScCA ]].


A series of << benzenesulfonamides >> incorporating cyanoacrylamide moieties (tyrphostine analogs) were assayed as inhibitors of the [[ β-carbonic anhydrase ]] (CA, EC 4.2.1.1) from Saccharomyces cerevisiae, ScCA.


A series of << benzenesulfonamides >> incorporating cyanoacrylamide moieties (tyrphostine analogs) were assayed as inhibitors of the β-carbonic anhydrase ([[ CA ]], EC 4.2.1.1) from Saccharomyces cerevisiae, ScCA.


A series of benzenesulfonamides incorporating << cyanoacrylamide >> moieties (tyrphostine analogs) were assayed as inhibitors of the β-carbonic anhydrase (CA, [[ EC 4.2.1.1 ]]) from Saccharomyces cerevisiae, ScCA.


A series of benzenesulfonamides incorporating << cyanoacrylamide >> moieties (tyrphostine analogs) were assayed as inhibitors of the β-carbonic anhydrase (CA, EC 4.2.1.1) from Saccharomyces cerevisiae, [[ ScCA ]].


A series of benzenesulfonamides incorporating << cyanoacrylamide >> moieties (tyrphostine analogs) were assayed as inhibitors of the [[ β-carbonic anhydrase ]] (CA, EC 4.2.1.1) from Saccharomyces cerevisiae, ScCA.


A series of benzenesulfonamides incorporating << cyanoacrylamide >> moieties (tyrphostine analogs) were assayed as inhibitors of the β-carbonic anhydrase ([[ CA ]], EC 4.2.1.1) from Saccharomyces cerevisiae, ScCA.


A series of benzenesulfonamides incorporating cyanoacrylamide moieties (<< tyrphostine >> analogs) were assayed as inhibitors of the β-carbonic anhydrase (CA, [[ EC 4.2.1.1 ]]) from Saccharomyces cerevisiae, ScCA.


A series of benzenesulfonamides incorporating cyanoacrylamide moieties (<< tyrphostine >> analogs) were assayed as inhibitors of the β-carbonic anhydrase (CA, EC 4.2.1.1) from Saccharomyces cerevisiae, [[ ScCA ]].


A series of benzenesulfonamides incorporating cyanoacrylamide moieties (<< tyrphostine >> analogs) were assayed as inhibitors of the [[ β-carbonic anhydrase ]] (CA, EC 4.2.1.1) from Saccharomyces cerevisiae, ScCA.


A series of benzenesulfonamides incorporating cyanoacrylamide moieties (<< tyrphostine >> analogs) were assayed as inhibitors of the β-carbonic anhydrase ([[ CA ]], EC 4.2.1.1) from Saccharomyces cerevisiae, ScCA.


<< Artemisinic acid >> inhibits melanogenesis through downregulation of C/EBP α-dependent expression of [[ HMG-CoA reductase ]] gene.


<< Artemisinic acid >> inhibits melanogenesis through downregulation of [[ C/EBP α ]]-dependent expression of HMG-CoA reductase gene.


The mRNA levels of << microphthalmia-associated transcription factor >> (MITF) and its downstream genes tyrosinase, tyrosinase-related protein (TRP)-1, and TRP-2 were reduced by [[ artemisinic acid ]] treatment.


The mRNA levels of microphthalmia-associated transcription factor (<< MITF >>) and its downstream genes tyrosinase, tyrosinase-related protein (TRP)-1, and TRP-2 were reduced by [[ artemisinic acid ]] treatment.


The mRNA levels of microphthalmia-associated transcription factor (MITF) and its downstream genes << tyrosinase >>, tyrosinase-related protein (TRP)-1, and TRP-2 were reduced by [[ artemisinic acid ]] treatment.


The mRNA levels of microphthalmia-associated transcription factor (MITF) and its downstream genes tyrosinase, << tyrosinase-related protein (TRP)-1 >>, and TRP-2 were reduced by [[ artemisinic acid ]] treatment.


The mRNA levels of microphthalmia-associated transcription factor (MITF) and its downstream genes tyrosinase, tyrosinase-related protein (TRP)-1, and << TRP-2 >> were reduced by [[ artemisinic acid ]] treatment.


Additionally, the mRNA levels of melanogenesis-related genes (<< c-KIT >>, stem cell factor (SCF), and macrophage migration inhibitory factor (MIF)) were down-regulated by [[ artemisinic acid ]].


Additionally, the mRNA levels of melanogenesis-related genes (c-KIT, << stem cell factor >> (SCF), and macrophage migration inhibitory factor (MIF)) were down-regulated by [[ artemisinic acid ]].


Additionally, the mRNA levels of melanogenesis-related genes (c-KIT, stem cell factor (<< SCF >>), and macrophage migration inhibitory factor (MIF)) were down-regulated by [[ artemisinic acid ]].


Additionally, the mRNA levels of melanogenesis-related genes (c-KIT, stem cell factor (SCF), and << macrophage migration inhibitory factor >> (MIF)) were down-regulated by [[ artemisinic acid ]].


Additionally, the mRNA levels of melanogenesis-related genes (c-KIT, stem cell factor (SCF), and macrophage migration inhibitory factor (<< MIF >>)) were down-regulated by [[ artemisinic acid ]].


Furthermore, cAMP production and << protein kinase A >> (PKA) activity were suppressed by [[ artemisinic acid ]].


Furthermore, cAMP production and protein kinase A (<< PKA >>) activity were suppressed by [[ artemisinic acid ]].


Moreover, attempts to elucidate a possible mechanism underlying the artemisinic acid-mediated effects revealed that << artemisinic acid >> regulated melanogenesis by inhibiting cholesterol synthesis through downregulation of the [[ hydroxymethylglutaryl CoA (HMG CoA) reductase ]] gene, which was mediated through reduced expression of the CCAAT/enhancer-binding protein (C/EBP) α gene.


Moreover, attempts to elucidate a possible mechanism underlying the artemisinic acid-mediated effects revealed that << artemisinic acid >> regulated melanogenesis by inhibiting cholesterol synthesis through downregulation of the hydroxymethylglutaryl CoA (HMG CoA) reductase gene, which was mediated through reduced expression of the [[ CCAAT/enhancer-binding protein (C/EBP) α ]] gene.


Taken together, these findings indicate that the inhibition of melanogenesis by << artemisinic acid >> occurs through reduced expression of the [[ HMG CoA reductase ]] gene, which is mediated by C/EBP α inhibition and suggest that artemisinic acid may be useful as a hyperpigmentation inhibitor.


Taken together, these findings indicate that the inhibition of melanogenesis by << artemisinic acid >> occurs through reduced expression of the HMG CoA reductase gene, which is mediated by [[ C/EBP α ]] inhibition and suggest that artemisinic acid may be useful as a hyperpigmentation inhibitor.


As determined by Western and Northern blot analyses, << 5 alpha-NET >> inhibited the P4-induced [[ UG ]] gene expression in a dose-dependent manner.


The estrogenic agent << 3 beta,5 alpha-NET >> and estradiol at a dose of 1.0 mg also inhibited the [[ UG ]] gene expression induced by P4.


The estrogenic agent 3 beta,5 alpha-NET and << estradiol >> at a dose of 1.0 mg also inhibited the [[ UG ]] gene expression induced by P4.


Both << 5 alpha-NET >> and 3 beta,5 alpha-NET blocked the [[ PR ]] down-regulation induced by P4 as assessed by Western and Northern blot methods.


Both 5 alpha-NET and << 3 beta,5 alpha-NET >> blocked the [[ PR ]] down-regulation induced by P4 as assessed by Western and Northern blot methods.


The inhibition of UG synthesis and << PR >> down-regulation by [[ 5 alpha-NET ]] and 3 beta,5 alpha-NET indicates that these NET metabolites possess antiprogestational properties.


The inhibition of << UG >> synthesis and PR down-regulation by [[ 5 alpha-NET ]] and 3 beta,5 alpha-NET indicates that these NET metabolites possess antiprogestational properties.


The inhibition of << UG >> synthesis and PR down-regulation by 5 alpha-NET and [[ 3 beta,5 alpha-NET ]] indicates that these NET metabolites possess antiprogestational properties.


The inhibition of UG synthesis and << PR >> down-regulation by 5 alpha-NET and [[ 3 beta,5 alpha-NET ]] indicates that these NET metabolites possess antiprogestational properties.


The inhibition of << UG >> synthesis and PR down-regulation by 5 alpha-NET and 3 beta,5 alpha-NET indicates that these [[ NET ]] metabolites possess antiprogestational properties.


The inhibition of UG synthesis and << PR >> down-regulation by 5 alpha-NET and 3 beta,5 alpha-NET indicates that these [[ NET ]] metabolites possess antiprogestational properties.


Meanwhile, autophagy was detected as early as 12 h after an exposure to low-dose << dioscin >>, as indicated by an up-regulated expression of [[ LC3-II ]] and beclin-1 proteins.


Meanwhile, autophagy was detected as early as 12 h after an exposure to low-dose << dioscin >>, as indicated by an up-regulated expression of LC3-II and [[ beclin-1 ]] proteins.


Treatment of A549 and H1299 cells with << dioscin >> caused a dose-dependent increase in ERK1/2 and [[ JNK1/2 ]] activity, accompanied with a decreased PI3K expression and decreased phosphorylation of Akt and mTOR.


Treatment of A549 and H1299 cells with << dioscin >> caused a dose-dependent increase in [[ ERK1/2 ]] and JNK1/2 activity, accompanied with a decreased PI3K expression and decreased phosphorylation of Akt and mTOR.


Treatment of A549 and H1299 cells with << dioscin >> caused a dose-dependent increase in ERK1/2 and JNK1/2 activity, accompanied with a decreased [[ PI3K ]] expression and decreased phosphorylation of Akt and mTOR.


Treatment of A549 and H1299 cells with << dioscin >> caused a dose-dependent increase in ERK1/2 and JNK1/2 activity, accompanied with a decreased PI3K expression and decreased phosphorylation of [[ Akt ]] and mTOR.


Treatment of A549 and H1299 cells with << dioscin >> caused a dose-dependent increase in ERK1/2 and JNK1/2 activity, accompanied with a decreased PI3K expression and decreased phosphorylation of Akt and [[ mTOR ]].


Our results showed that << 2-hydroxy-3-methylanthraquinone >> decreased phosphorylation-ERK1/2 (p-ERK1/2), and increased [[ p-p38MAPK ]], but did not affect expressions of p-JNK1/2 in U937 cells.


Moreover, treatment of U937 cells with << 2-hydroxy-3-methylanthraquinone >> resulted in activation of [[ caspase-3 ]].


Furthermore, PD98059 (ERK1/2 inhibitor) significantly enhanced 2-hydroxy-3-methylanthraquinone-induced apoptosis in U937 cells, whereas caspase-3 inhibitor or << SB203580 >> ([[ p-p38MAPK ]] inhibitor), decreased apoptosis in U937 cells.


Taken together, our study for the first time suggests that << 2-hydroxy-3-methylanthraquinone >> is able to enhance apoptosis of U937 cells, at least in part, through activation of [[ p-p38MAPK ]] and downregulation of p-ERK1/2.


<< Ribonucleotide reductase >> activity was found to be strongly increased in the [[ gemcitabine ]]-selected line and purine nucleoside phosphorylase was increased in the 2-chlorodeoxyadenosine-selected line.


Ribonucleotide reductase activity was found to be strongly increased in the gemcitabine-selected line and << purine nucleoside phosphorylase >> was increased in the [[ 2-chlorodeoxyadenosine ]]-selected line.


A new series of << N2-substituted-5-(p-toluenesulfonylamino)phthalimide >> analogues as [[ α-glucosidase ]] inhibitors.


Several members of a new family of non-sugar-type << α-glycosidase >> inhibitors, bearing a [[ 5-(p-toluenesulfonylamino)phthalimide ]] moiety and various substituent at the N2 position, were synthesized and their activities were investigated.


Structure-activity relationship studies indicated that << 5-(p-toluenesulfonylamino)phthalimide >> moiety is a favorable scaffold to exert the [[ α-glucosidase ]] inhibitory activity and substituents at the N2 position have considerable influence on the efficacy of the inhibition activities.


The lysosomal inhibitor << chloroquine >> significantly increased [[ RCAN1 ]] accumulation in +/+ cells, consistent with the hypothesis that higher lysosomal pH impairs RCAN1 degradation, leading to a higher RCAN1/NFATc1 ratio and consequently NFATc1 inhibition.


Here, we have now found that activation of << p38 >> MAPK by [[ anisomycin ]] potentiated induction of CYP2B6 mRNA by CAR ligand in HepG2 cells to levels observed in ligand-treated human primary hepatocytes.


Here, we have now found that activation of p38 << MAPK >> by [[ anisomycin ]] potentiated induction of CYP2B6 mRNA by CAR ligand in HepG2 cells to levels observed in ligand-treated human primary hepatocytes.


Here, we have now found that activation of p38 MAPK by << anisomycin >> potentiated induction of [[ CYP2B6 ]] mRNA by CAR ligand in HepG2 cells to levels observed in ligand-treated human primary hepatocytes.


siRNA knockdown of p38 MAPK abrogated the ability of << anisomycin >> to synergistically induce [[ CYP2B6 ]] mRNA.


In addition to << CYP2B6 >>, [[ anisomycin ]] co-treatment potentiated an increase in CYP2A7 and CYP2C9 mRNAs but not CYP3A4 or UDP-glucuronosyltransferase 1A1 mRNAs.


In addition to CYP2B6, << anisomycin >> co-treatment potentiated an increase in [[ CYP2A7 ]] and CYP2C9 mRNAs but not CYP3A4 or UDP-glucuronosyltransferase 1A1 mRNAs.


In addition to CYP2B6, << anisomycin >> co-treatment potentiated an increase in CYP2A7 and [[ CYP2C9 ]] mRNAs but not CYP3A4 or UDP-glucuronosyltransferase 1A1 mRNAs.


No effects were observed when << fenclozic acid >> was assessed for P450-dependent and P450-independent cytotoxicity to THLE cell lines, time-dependent inhibition of five major [[ human cytochrome P450 ]] enzymes, inhibition of the biliary efflux transporters BSEP and MRP2 or mitochondrial toxicity to THLE or HepG2 cells.


No effects were observed when << fenclozic acid >> was assessed for P450-dependent and P450-independent cytotoxicity to THLE cell lines, time-dependent inhibition of five major human cytochrome P450 enzymes, inhibition of the biliary [[ efflux transporters ]] BSEP and MRP2 or mitochondrial toxicity to THLE or HepG2 cells.


No effects were observed when << fenclozic acid >> was assessed for P450-dependent and P450-independent cytotoxicity to THLE cell lines, time-dependent inhibition of five major human cytochrome P450 enzymes, inhibition of the biliary efflux transporters [[ BSEP ]] and MRP2 or mitochondrial toxicity to THLE or HepG2 cells.


No effects were observed when << fenclozic acid >> was assessed for P450-dependent and P450-independent cytotoxicity to THLE cell lines, time-dependent inhibition of five major human cytochrome P450 enzymes, inhibition of the biliary efflux transporters BSEP and [[ MRP2 ]] or mitochondrial toxicity to THLE or HepG2 cells.


<< Auranofin >>, as an anti-rheumatic gold compound, suppresses LPS-induced homodimerization of [[ TLR4 ]].


Our results demonstrated that << auranofin >> suppressed TLR4-mediated activation of transcription factors, NF-kappaB and IRF3, and expression of [[ COX-2 ]], a pro-inflammatory enzyme.


Our results demonstrated that << auranofin >> suppressed [[ TLR4 ]]-mediated activation of transcription factors, NF-kappaB and IRF3, and expression of COX-2, a pro-inflammatory enzyme.


Our results demonstrated that << auranofin >> suppressed TLR4-mediated activation of transcription factors, [[ NF-kappaB ]] and IRF3, and expression of COX-2, a pro-inflammatory enzyme.


Our results demonstrated that << auranofin >> suppressed TLR4-mediated activation of transcription factors, NF-kappaB and [[ IRF3 ]], and expression of COX-2, a pro-inflammatory enzyme.


This suppression was well correlated with the inhibitory effect of << auranofin >> on the homodimerization of [[ TLR4 ]] induced by an agonist.


Furthermore, << auranofin >> inhibited [[ NF-kappaB ]] activation induced by MyD88-dependent downstream signaling components of TLR4, MyD88, IKKbeta, and p65.


<< IRF3 >> activation induced by MyD88-independent signaling components, TRIF and TBK1, was also downregulated by [[ auranofin ]].


IRF3 activation induced by MyD88-independent signaling components, << TRIF >> and TBK1, was also downregulated by [[ auranofin ]].


IRF3 activation induced by MyD88-independent signaling components, TRIF and << TBK1 >>, was also downregulated by [[ auranofin ]].


Our results first demonstrate that << auranofin >> suppresses the multiple steps in [[ TLR4 ]] signaling, especially the homodimerization of TLR4.


Our results first demonstrate that << auranofin >> suppresses the multiple steps in TLR4 signaling, especially the homodimerization of [[ TLR4 ]].


The results suggest that the suppression of << TLR4 >> activity by auranofin may be the molecular mechanism through which [[ auranofin ]] exerts anti-rheumatic activity.


The results suggest that the suppression of << TLR4 >> activity by [[ auranofin ]] may be the molecular mechanism through which auranofin exerts anti-rheumatic activity.


<< Vandetanib >> (Caprelsa(®), AstraZeneca) is a once-daily oral tyrosine kinase inhibitor that selectively inhibits signalling mediated by growth-factor receptor tyrosine kinase RET (constitutively activated in roughly 60 % of all MTCs), vascular endothelial growth-factor receptors 2 and 3, and [[ epidermal growth-factor receptors ]].


<< Vandetanib >> (Caprelsa(®), AstraZeneca) is a once-daily oral [[ tyrosine kinase ]] inhibitor that selectively inhibits signalling mediated by growth-factor receptor tyrosine kinase RET (constitutively activated in roughly 60 % of all MTCs), vascular endothelial growth-factor receptors 2 and 3, and epidermal growth-factor receptors.


<< Vandetanib >> (Caprelsa(®), AstraZeneca) is a once-daily oral tyrosine kinase inhibitor that selectively inhibits signalling mediated by [[ growth-factor receptor tyrosine kinase ]] RET (constitutively activated in roughly 60 % of all MTCs), vascular endothelial growth-factor receptors 2 and 3, and epidermal growth-factor receptors.


<< Vandetanib >> (Caprelsa(®), AstraZeneca) is a once-daily oral tyrosine kinase inhibitor that selectively inhibits signalling mediated by growth-factor receptor tyrosine kinase [[ RET ]] (constitutively activated in roughly 60 % of all MTCs), vascular endothelial growth-factor receptors 2 and 3, and epidermal growth-factor receptors.


Vandetanib (<< Caprelsa >>(®), AstraZeneca) is a once-daily oral tyrosine kinase inhibitor that selectively inhibits signalling mediated by growth-factor receptor tyrosine kinase RET (constitutively activated in roughly 60 % of all MTCs), vascular endothelial growth-factor receptors 2 and 3, and [[ epidermal growth-factor receptors ]].


Vandetanib (<< Caprelsa >>(®), AstraZeneca) is a once-daily oral [[ tyrosine kinase ]] inhibitor that selectively inhibits signalling mediated by growth-factor receptor tyrosine kinase RET (constitutively activated in roughly 60 % of all MTCs), vascular endothelial growth-factor receptors 2 and 3, and epidermal growth-factor receptors.


One exception is << tranexamic acid >> (TXA), which, as a lysine mimetic, inhibits binding of [[ plasminogen ]] to fibrin.


One exception is << tranexamic acid >> (TXA), which, as a lysine mimetic, inhibits binding of plasminogen to [[ fibrin ]].


One exception is tranexamic acid (<< TXA >>), which, as a lysine mimetic, inhibits binding of [[ plasminogen ]] to fibrin.


One exception is tranexamic acid (<< TXA >>), which, as a lysine mimetic, inhibits binding of plasminogen to [[ fibrin ]].


One exception is tranexamic acid (TXA), which, as a << lysine >> mimetic, inhibits binding of [[ plasminogen ]] to fibrin.


One exception is tranexamic acid (TXA), which, as a << lysine >> mimetic, inhibits binding of plasminogen to [[ fibrin ]].


Coupling this computational technique with a high-quality low-throughput screen identified << 5-(4-piperidyl)-3-isoxazolol >> (4-PIOL) as a potent [[ plasminogen ]] binding inhibitor with the potential for the treatment of various bleeding disorders.


Coupling this computational technique with a high-quality low-throughput screen identified 5-(4-piperidyl)-3-isoxazolol (<< 4-PIOL >>) as a potent [[ plasminogen ]] binding inhibitor with the potential for the treatment of various bleeding disorders.


Epididymal tissue from wild-type mice responded in vitro to << noradrenaline >> and isoprenaline with increased glycerol release, reduced [[ IL-6 ]] release, and increased cAMP accumulation.


Epididymal tissue from wild-type mice responded in vitro to noradrenaline and << isoprenaline >> with increased glycerol release, reduced [[ IL-6 ]] release, and increased cAMP accumulation.


<< Phospholipase A2 >> inhibitors [[ p-bromophenacyl bromide ]] and arachidonyl trifluoromethyl ketone suppressed interleukin-2 (IL-2) expression in murine primary splenocytes.


Phospholipase A2 inhibitors << p-bromophenacyl bromide >> and arachidonyl trifluoromethyl ketone suppressed [[ interleukin-2 ]] (IL-2) expression in murine primary splenocytes.


Phospholipase A2 inhibitors << p-bromophenacyl bromide >> and arachidonyl trifluoromethyl ketone suppressed interleukin-2 ([[ IL-2 ]]) expression in murine primary splenocytes.


Phospholipase A2 inhibitors p-bromophenacyl bromide and << arachidonyl trifluoromethyl ketone >> suppressed [[ interleukin-2 ]] (IL-2) expression in murine primary splenocytes.


Phospholipase A2 inhibitors p-bromophenacyl bromide and << arachidonyl trifluoromethyl ketone >> suppressed interleukin-2 ([[ IL-2 ]]) expression in murine primary splenocytes.


<< Phospholipase A2 >> inhibitors p-bromophenacyl bromide and [[ arachidonyl trifluoromethyl ketone ]] suppressed interleukin-2 (IL-2) expression in murine primary splenocytes.


Therefore, the objective of the present study was to investigate the effects of << PLA2 >> inhibitors [[ p-bromophenacyl bromide ]] (BPB) and arachidonyl trifluoromethyl ketone (AACOCF3) on interleukin-2 (IL-2) expression in murine primary splenocytes.


Therefore, the objective of the present study was to investigate the effects of << PLA2 >> inhibitors p-bromophenacyl bromide ([[ BPB ]]) and arachidonyl trifluoromethyl ketone (AACOCF3) on interleukin-2 (IL-2) expression in murine primary splenocytes.


Therefore, the objective of the present study was to investigate the effects of << PLA2 >> inhibitors p-bromophenacyl bromide (BPB) and [[ arachidonyl trifluoromethyl ketone ]] (AACOCF3) on interleukin-2 (IL-2) expression in murine primary splenocytes.


Therefore, the objective of the present study was to investigate the effects of << PLA2 >> inhibitors p-bromophenacyl bromide (BPB) and arachidonyl trifluoromethyl ketone ([[ AACOCF3 ]]) on interleukin-2 (IL-2) expression in murine primary splenocytes.


Pretreatment of the splenocytes with both BPB and AACOCF3 suppressed << phorbol 12-myristate 13-acetate >> plus ionomycin-induced [[ IL-2 ]] secretion in a concentration-dependent manner.


Pretreatment of the splenocytes with both << BPB >> and AACOCF3 suppressed phorbol 12-myristate 13-acetate plus ionomycin-induced [[ IL-2 ]] secretion in a concentration-dependent manner.


Pretreatment of the splenocytes with both BPB and << AACOCF3 >> suppressed phorbol 12-myristate 13-acetate plus ionomycin-induced [[ IL-2 ]] secretion in a concentration-dependent manner.


Inhibition > 90% of << IL-2 >> secretion was observed at 1 microM [[ BPB ]] and 10 microM AACOCF3 compared to the respective vehicle control.


Inhibition > 90% of << IL-2 >> secretion was observed at 1 microM BPB and 10 microM [[ AACOCF3 ]] compared to the respective vehicle control.


Likewise, << IL-2 >> steady-state mRNA expression was inhibited by both PLA2 inhibitors in a concentration-dependent fashion with > 90% inhibition at 1 microM [[ BPB ]] and 20 microM AACOCF3.


Likewise, << IL-2 >> steady-state mRNA expression was inhibited by both PLA2 inhibitors in a concentration-dependent fashion with > 90% inhibition at 1 microM BPB and 20 microM [[ AACOCF3 ]].


Likewise, IL-2 steady-state mRNA expression was inhibited by both << PLA2 >> inhibitors in a concentration-dependent fashion with > 90% inhibition at 1 microM [[ BPB ]] and 20 microM AACOCF3.


Likewise, IL-2 steady-state mRNA expression was inhibited by both << PLA2 >> inhibitors in a concentration-dependent fashion with > 90% inhibition at 1 microM BPB and 20 microM [[ AACOCF3 ]].


Taken together, these data demonstrated that PLA2 inhibitors << BPB >> and AACOCF3 are robust inhibitors of [[ IL-2 ]] expression at both the mRNA and protein levels in murine splenocytes.


Taken together, these data demonstrated that PLA2 inhibitors BPB and << AACOCF3 >> are robust inhibitors of [[ IL-2 ]] expression at both the mRNA and protein levels in murine splenocytes.


Taken together, these data demonstrated that << PLA2 >> inhibitors [[ BPB ]] and AACOCF3 are robust inhibitors of IL-2 expression at both the mRNA and protein levels in murine splenocytes.


Taken together, these data demonstrated that << PLA2 >> inhibitors BPB and [[ AACOCF3 ]] are robust inhibitors of IL-2 expression at both the mRNA and protein levels in murine splenocytes.


The two basic mainstays of gastrointestinal stromal tumours (GIST) treatment are surgery and << imatinib >>, a selective [[ tyrosine kinase ]] inhibitor that allows achieving a stable or responding disease in about 80% of patients with unresectable/metastatic GIST.


We have previously reported that << TZDs >> reduce estrogen synthesis by inhibiting [[ aromatase ]] activity in human granulosa cells (HGC).


We have previously reported that TZDs reduce << estrogen >> synthesis by inhibiting [[ aromatase ]] activity in human granulosa cells (HGC).


We studied mouse osteoblasts alone or in a co-culture with HGC to determine whether << TZD >> inhibition of [[ aromatase ]] plays a role in their effects on bone metabolism.


<< TZDs >> also inhibited [[ alkaline phosphatase ]] activity (58-75%, p<0.046) and osteocalcin production (52-75%, p<0.031).


<< TZDs >> also inhibited alkaline phosphatase activity (58-75%, p<0.046) and [[ osteocalcin ]] production (52-75%, p<0.031).


<< TZD >> effects on osteoblast viability, oleic acid uptake, alkaline phosphatase and osteocalcin production are independent of their effects on [[ aromatase ]].


Carnitine acetyltransferases (<< CrAT >>) catalyze the reversible conversion of acetyl-CoA and carnitine to [[ acetylcarnitine ]] and free CoA.


Carnitine acetyltransferases (<< CrAT >>) catalyze the reversible conversion of [[ acetyl-CoA ]] and carnitine to acetylcarnitine and free CoA.


Carnitine acetyltransferases (<< CrAT >>) catalyze the reversible conversion of acetyl-CoA and [[ carnitine ]] to acetylcarnitine and free CoA.


<< Carnitine acetyltransferases >> (CrAT) catalyze the reversible conversion of [[ acetyl-CoA ]] and carnitine to acetylcarnitine and free CoA.


<< Carnitine acetyltransferases >> (CrAT) catalyze the reversible conversion of acetyl-CoA and [[ carnitine ]] to acetylcarnitine and free CoA.


<< Carnitine acetyltransferases >> (CrAT) catalyze the reversible conversion of acetyl-CoA and carnitine to [[ acetylcarnitine ]] and free CoA.


The << M564G >> mutated CrAT showed higher activity toward longer chain acyl-CoAs: activity toward myristoyl-CoA was 1250-fold higher than that of the wild-type CrAT, and lower activity toward its natural substrate, [[ acetyl-CoA ]].


The M564G mutated << CrAT >> showed higher activity toward longer chain acyl-CoAs: activity toward myristoyl-CoA was 1250-fold higher than that of the wild-type CrAT, and lower activity toward its natural substrate, [[ acetyl-CoA ]].


The M564G mutated CrAT showed higher activity toward longer chain acyl-CoAs: activity toward myristoyl-CoA was 1250-fold higher than that of the wild-type << CrAT >>, and lower activity toward its natural substrate, [[ acetyl-CoA ]].


The << M564G >> mutated CrAT showed higher activity toward longer chain [[ acyl-CoAs ]]: activity toward myristoyl-CoA was 1250-fold higher than that of the wild-type CrAT, and lower activity toward its natural substrate, acetyl-CoA.


The M564G mutated << CrAT >> showed higher activity toward longer chain [[ acyl-CoAs ]]: activity toward myristoyl-CoA was 1250-fold higher than that of the wild-type CrAT, and lower activity toward its natural substrate, acetyl-CoA.


The M564G mutated CrAT showed higher activity toward longer chain << acyl-CoAs >>: activity toward myristoyl-CoA was 1250-fold higher than that of the wild-type [[ CrAT ]], and lower activity toward its natural substrate, acetyl-CoA.


The << M564G >> mutated CrAT showed higher activity toward longer chain acyl-CoAs: activity toward [[ myristoyl-CoA ]] was 1250-fold higher than that of the wild-type CrAT, and lower activity toward its natural substrate, acetyl-CoA.


The M564G mutated << CrAT >> showed higher activity toward longer chain acyl-CoAs: activity toward [[ myristoyl-CoA ]] was 1250-fold higher than that of the wild-type CrAT, and lower activity toward its natural substrate, acetyl-CoA.


The M564G mutated CrAT showed higher activity toward longer chain acyl-CoAs: activity toward << myristoyl-CoA >> was 1250-fold higher than that of the wild-type [[ CrAT ]], and lower activity toward its natural substrate, acetyl-CoA.


Kinetic constants of the mutant << CrAT >> showed modification in favor of longer [[ acyl-CoAs ]] as substrates.


In the reverse case, mutation of the orthologous glycine (Gly553) to methionine in << carnitine octanoyltransferase >> (COT) decreased activity toward its natural substrates, medium- and long-chain [[ acyl-CoAs ]], and increased activity toward short-chain acyl-CoAs.


In the reverse case, mutation of the orthologous glycine (Gly553) to methionine in carnitine octanoyltransferase (<< COT >>) decreased activity toward its natural substrates, medium- and long-chain [[ acyl-CoAs ]], and increased activity toward short-chain acyl-CoAs.


In the reverse case, mutation of the orthologous glycine (Gly553) to methionine in << carnitine octanoyltransferase >> (COT) decreased activity toward its natural substrates, medium- and long-chain acyl-CoAs, and increased activity toward short-chain [[ acyl-CoAs ]].


In the reverse case, mutation of the orthologous glycine (Gly553) to methionine in carnitine octanoyltransferase (<< COT >>) decreased activity toward its natural substrates, medium- and long-chain acyl-CoAs, and increased activity toward short-chain [[ acyl-CoAs ]].


We conclude that Met564 blocks the entry of medium- and long-chain << acyl-CoAs >> to the catalytic site of [[ CrAT ]].


Catecholamines (<< adrenaline >>, noradrenaline and dopamine) are potent inhibitors of phenylalanine 4-monooxygenase ([[ phenylalanine hydroxylase ]], EC 1.14.16.1).


Catecholamines (<< adrenaline >>, noradrenaline and dopamine) are potent inhibitors of phenylalanine 4-monooxygenase (phenylalanine hydroxylase, [[ EC 1.14.16.1 ]]).


Catecholamines (<< adrenaline >>, noradrenaline and dopamine) are potent inhibitors of [[ phenylalanine 4-monooxygenase ]] (phenylalanine hydroxylase, EC 1.14.16.1).


Catecholamines (adrenaline, << noradrenaline >> and dopamine) are potent inhibitors of phenylalanine 4-monooxygenase ([[ phenylalanine hydroxylase ]], EC 1.14.16.1).


Catecholamines (adrenaline, << noradrenaline >> and dopamine) are potent inhibitors of phenylalanine 4-monooxygenase (phenylalanine hydroxylase, [[ EC 1.14.16.1 ]]).


Catecholamines (adrenaline, << noradrenaline >> and dopamine) are potent inhibitors of [[ phenylalanine 4-monooxygenase ]] (phenylalanine hydroxylase, EC 1.14.16.1).


Catecholamines (adrenaline, noradrenaline and << dopamine >>) are potent inhibitors of phenylalanine 4-monooxygenase ([[ phenylalanine hydroxylase ]], EC 1.14.16.1).


Catecholamines (adrenaline, noradrenaline and << dopamine >>) are potent inhibitors of phenylalanine 4-monooxygenase (phenylalanine hydroxylase, [[ EC 1.14.16.1 ]]).


Catecholamines (adrenaline, noradrenaline and << dopamine >>) are potent inhibitors of [[ phenylalanine 4-monooxygenase ]] (phenylalanine hydroxylase, EC 1.14.16.1).


<< Catecholamines >> (adrenaline, noradrenaline and dopamine) are potent inhibitors of phenylalanine 4-monooxygenase ([[ phenylalanine hydroxylase ]], EC 1.14.16.1).


<< Catecholamines >> (adrenaline, noradrenaline and dopamine) are potent inhibitors of phenylalanine 4-monooxygenase (phenylalanine hydroxylase, [[ EC 1.14.16.1 ]]).


<< Catecholamines >> (adrenaline, noradrenaline and dopamine) are potent inhibitors of [[ phenylalanine 4-monooxygenase ]] (phenylalanine hydroxylase, EC 1.14.16.1).


Central and peripheral administration of << kisspeptin >> stimulates the hypothalamic-pituitary-gonadal (HPG) axis whilst pre-administration of a [[ gonadotrophin releasing hormone ]] (GnRH) antagonist abolishes this effect.


Central and peripheral administration of << kisspeptin >> stimulates the hypothalamic-pituitary-gonadal (HPG) axis whilst pre-administration of a gonadotrophin releasing hormone ([[ GnRH ]]) antagonist abolishes this effect.


<< Dexamethasone >> (DEX), betamethasone (BM), and their esterified-derivatives had full transrepression agonistic activity in a reporter assay using CV-1 cells transfected with either [[ human or rat GR ]].


Dexamethasone (<< DEX >>), betamethasone (BM), and their esterified-derivatives had full transrepression agonistic activity in a reporter assay using CV-1 cells transfected with either [[ human or rat GR ]].


Dexamethasone (DEX), << betamethasone >> (BM), and their esterified-derivatives had full transrepression agonistic activity in a reporter assay using CV-1 cells transfected with either [[ human or rat GR ]].


Dexamethasone (DEX), betamethasone (<< BM >>), and their esterified-derivatives had full transrepression agonistic activity in a reporter assay using CV-1 cells transfected with either [[ human or rat GR ]].


The esterified-BM, however, had only partial transactivation agonistic activity in cells transfected with << rat GR >>, whereas [[ BM ]] and esterified-DEX had full transactivation agonistic activity.


The esterified-BM, however, had only partial transactivation agonistic activity in cells transfected with << rat GR >>, whereas BM and esterified-[[ DEX ]] had full transactivation agonistic activity.


The esterified-<< BM >>, however, had only partial transactivation agonistic activity in cells transfected with [[ rat GR ]], whereas BM and esterified-DEX had full transactivation agonistic activity.


Moreover, in rat hepatoma H4-II-E cells, the esterified-<< BM >> failed to induce tyrosine aminotransferase, which is regulated by [[ GR ]]-mediated transactivation activity.


Consistent with the weak transactivation activity of esterified-<< BM >> mediated by [[ rat GR ]], there were few side effects, evaluated by thymus involution and body weight loss, in an antigen-induced asthmatic model in rats.


Moreover, << IGFBP-rP2 >> noticeably increased in response to TGF-beta1 and [[ all-trans retinoic acid ]] (atRA) in HPEC and PC-3 cells, and it decreased in response to IGF-I in HPEC.


Moreover, << IGFBP-rP2 >> noticeably increased in response to TGF-beta1 and all-trans retinoic acid ([[ atRA ]]) in HPEC and PC-3 cells, and it decreased in response to IGF-I in HPEC.


Although the data collected on << IGFBP-rP3 >> in prostate are modest, its role as a growth stimulator and/or protooncogene is supported by its preferential expression in cancerous cells and its down-regulation by [[ atRA ]].


On the basis of FIP1L1-PDGFRa fusion gene hypereosinophilic syndrome would be classified as a clonal disease and in the FIP1L1-PDGFRa positive cases the << tyrosine kinase >> inhibitor [[ imatinib mesylate ]] (Glivec) would be effective.


Transport by << OATP1B1 >> and OATP1B3 enhances the cytotoxicity of epigallocatechin 3-O-gallate and several [[ quercetin ]] derivatives.


Transport by OATP1B1 and << OATP1B3 >> enhances the cytotoxicity of epigallocatechin 3-O-gallate and several [[ quercetin ]] derivatives.


Transport by << OATP1B1 >> and OATP1B3 enhances the cytotoxicity of [[ epigallocatechin 3-O-gallate ]] and several quercetin derivatives.


Transport by OATP1B1 and << OATP1B3 >> enhances the cytotoxicity of [[ epigallocatechin 3-O-gallate ]] and several quercetin derivatives.


Uptake of the radiolabeled model substrates << estradiol 17β-glucuronide >>, estrone 3-sulfate, and dehydroepiandrosterone sulfate (DHEAS) was determined in the absence and presence of compounds 1-6 using Chinese hamster ovary (CHO) cells stably expressing either [[ OATP1B1 ]] or OATP1B3.


Uptake of the radiolabeled model substrates << estradiol 17β-glucuronide >>, estrone 3-sulfate, and dehydroepiandrosterone sulfate (DHEAS) was determined in the absence and presence of compounds 1-6 using Chinese hamster ovary (CHO) cells stably expressing either OATP1B1 or [[ OATP1B3 ]].


Uptake of the radiolabeled model substrates estradiol 17β-glucuronide, << estrone 3-sulfate >>, and dehydroepiandrosterone sulfate (DHEAS) was determined in the absence and presence of compounds 1-6 using Chinese hamster ovary (CHO) cells stably expressing either [[ OATP1B1 ]] or OATP1B3.


Uptake of the radiolabeled model substrates estradiol 17β-glucuronide, << estrone 3-sulfate >>, and dehydroepiandrosterone sulfate (DHEAS) was determined in the absence and presence of compounds 1-6 using Chinese hamster ovary (CHO) cells stably expressing either OATP1B1 or [[ OATP1B3 ]].


Uptake of the radiolabeled model substrates estradiol 17β-glucuronide, estrone 3-sulfate, and << dehydroepiandrosterone sulfate >> (DHEAS) was determined in the absence and presence of compounds 1-6 using Chinese hamster ovary (CHO) cells stably expressing either [[ OATP1B1 ]] or OATP1B3.


Uptake of the radiolabeled model substrates estradiol 17β-glucuronide, estrone 3-sulfate, and << dehydroepiandrosterone sulfate >> (DHEAS) was determined in the absence and presence of compounds 1-6 using Chinese hamster ovary (CHO) cells stably expressing either OATP1B1 or [[ OATP1B3 ]].


Uptake of the radiolabeled model substrates estradiol 17β-glucuronide, estrone 3-sulfate, and dehydroepiandrosterone sulfate (<< DHEAS >>) was determined in the absence and presence of compounds 1-6 using Chinese hamster ovary (CHO) cells stably expressing either [[ OATP1B1 ]] or OATP1B3.


Uptake of the radiolabeled model substrates estradiol 17β-glucuronide, estrone 3-sulfate, and dehydroepiandrosterone sulfate (<< DHEAS >>) was determined in the absence and presence of compounds 1-6 using Chinese hamster ovary (CHO) cells stably expressing either OATP1B1 or [[ OATP1B3 ]].


Compound 6 stimulated OATP1B3-mediated << estradiol 17β-glucuronide >> uptake by increasing the apparent affinity of [[ OATP1B3 ]] for its substrate.


Compound 6 stimulated << OATP1B3 >>-mediated [[ estradiol 17β-glucuronide ]] uptake by increasing the apparent affinity of OATP1B3 for its substrate.


Cytotoxicity assays demonstrated that << epigallocatechin 3-O-gallate >> (EGCG) and most of compounds 1-6 killed preferentially [[ OATP ]]-expressing CHO cells.


Cytotoxicity assays demonstrated that epigallocatechin 3-O-gallate (<< EGCG >>) and most of compounds 1-6 killed preferentially [[ OATP ]]-expressing CHO cells.


EGCG, 1, and 3 were the most potent cytotoxic compounds, with << EGCG >> and 3 selectively killing [[ OATP1B3 ]]-expressing cells.


<< Reboxetine >>, a selective norepinephrine reuptake inhibitor, exhibits high affinity and selectivity for the [[ human norepinephrine transporter ]].


We previously employed a chemical genomic strategy to identify a novel small molecule, << MAC13243 >>, as a likely inhibitor of the [[ bacterial lipoprotein ]] targeting chaperone, LolA.


We previously employed a chemical genomic strategy to identify a novel small molecule, << MAC13243 >>, as a likely inhibitor of the bacterial lipoprotein targeting [[ chaperone ]], LolA.


We previously employed a chemical genomic strategy to identify a novel small molecule, << MAC13243 >>, as a likely inhibitor of the bacterial lipoprotein targeting chaperone, [[ LolA ]].


Our results showed that low dose << BPA >> and E2 could influence the mammosphere area of iDMECs and upregulate the expression level of [[ Oct4 ]] and Nanog proteins, while only BPA could downregulate the expression of E-cadherin protein.


Our results showed that low dose << BPA >> and E2 could influence the mammosphere area of iDMECs and upregulate the expression level of Oct4 and [[ Nanog ]] proteins, while only BPA could downregulate the expression of E-cadherin protein.


Our results showed that low dose BPA and E2 could influence the mammosphere area of iDMECs and upregulate the expression level of Oct4 and Nanog proteins, while only << BPA >> could downregulate the expression of [[ E-cadherin ]] protein.


To this end, 158N murine oligodendrocytes were treated with << 7KC >> or 7βOHC inducing an apoptotic mode of cell death characterized by condensation/fragmentation of the nuclei, dephosphorylation of Akt and GSK3, mitochondrial depolarization involving [[ Mcl-1 ]], and caspase-3 activation.


To this end, 158N murine oligodendrocytes were treated with << 7KC >> or 7βOHC inducing an apoptotic mode of cell death characterized by condensation/fragmentation of the nuclei, dephosphorylation of Akt and GSK3, mitochondrial depolarization involving Mcl-1, and [[ caspase-3 ]] activation.


To this end, 158N murine oligodendrocytes were treated with 7KC or << 7βOHC >> inducing an apoptotic mode of cell death characterized by condensation/fragmentation of the nuclei, dephosphorylation of Akt and GSK3, mitochondrial depolarization involving [[ Mcl-1 ]], and caspase-3 activation.


To this end, 158N murine oligodendrocytes were treated with 7KC or << 7βOHC >> inducing an apoptotic mode of cell death characterized by condensation/fragmentation of the nuclei, dephosphorylation of Akt and GSK3, mitochondrial depolarization involving Mcl-1, and [[ caspase-3 ]] activation.


Thus, in 158N cells, the ability of << oxysterols >> to trigger a mode of cell death by apoptosis involving [[ GSK-3 ]] and caspase-3 activation is independent of the increase in the Ca(2+) level and of their accumulation in lipid raft microdomains.


Thus, in 158N cells, the ability of << oxysterols >> to trigger a mode of cell death by apoptosis involving GSK-3 and [[ caspase-3 ]] activation is independent of the increase in the Ca(2+) level and of their accumulation in lipid raft microdomains.


<< Sulindac sulfide >> inhibits epidermal growth factor-induced phosphorylation of extracellular-regulated kinase 1/2 and [[ Bad ]] in human colon cancer cells.


<< Sulindac sulfide >> inhibits [[ epidermal growth factor ]]-induced phosphorylation of extracellular-regulated kinase 1/2 and Bad in human colon cancer cells.


<< Sulindac >> and selective [[ cyclooxygenase (COX)-2 ]] inhibitors cause regression of colonic polyps in familial polyposis patients.


<< Sulindac >> metabolites and other nonsteroidal anti-inflammatory drugs selectively inhibit [[ ERK1/2 ]] phosphorylation in human colon cancer cells.


EGF-stimulated phosphorylation of ERK and Bad is blocked by pretreatment with << U0126 >>, a selective [[ MAP kinase kinase (MKK)1/2 ]] inhibitor.


<< EGF >>-stimulated phosphorylation of ERK and Bad is blocked by pretreatment with [[ U0126 ]], a selective MAP kinase kinase (MKK)1/2 inhibitor.


EGF-stimulated phosphorylation of << ERK >> and Bad is blocked by pretreatment with [[ U0126 ]], a selective MAP kinase kinase (MKK)1/2 inhibitor.


EGF-stimulated phosphorylation of ERK and << Bad >> is blocked by pretreatment with [[ U0126 ]], a selective MAP kinase kinase (MKK)1/2 inhibitor.


Similarly, pretreatment with << sulindac sulfide >> blocks the ability of EGF to induce ERK1/2 and Bad phosphorylation, but also down-regulates total [[ Bad ]] but not ERK1/2 protein levels.


Similarly, pretreatment with << sulindac sulfide >> blocks the ability of [[ EGF ]] to induce ERK1/2 and Bad phosphorylation, but also down-regulates total Bad but not ERK1/2 protein levels.


Similarly, pretreatment with << sulindac sulfide >> blocks the ability of EGF to induce ERK1/2 and [[ Bad ]] phosphorylation, but also down-regulates total Bad but not ERK1/2 protein levels.


The ability of << sulindac >> to block [[ ERK1/2 ]] signaling by the EGF receptor may account for at least part of its potent growth-inhibitory effects against cancer cells.


The ability of << sulindac >> to block ERK1/2 signaling by the [[ EGF receptor ]] may account for at least part of its potent growth-inhibitory effects against cancer cells.


After inflammation was established mice were dosed with the << H4R >> antagonist, [[ JNJ 7777120 ]], or anti-IL-13 antibody for comparison.


Development and validation of a non-radioactive << DNA polymerase >> assay for studying cytomegalovirus resistance to [[ foscarnet ]].


The activity of << polymerases >> containing mutations known to confer resistance to foscarnet (V715M, T700A and N495K) was inhibited by concentrations of [[ foscarnet ]] eight to 14 times higher than those required to inhibit wild-type polymerases.


The activity of polymerases containing mutations known to confer resistance to foscarnet (<< V715M >>, T700A and N495K) was inhibited by concentrations of [[ foscarnet ]] eight to 14 times higher than those required to inhibit wild-type polymerases.


The activity of polymerases containing mutations known to confer resistance to foscarnet (V715M, << T700A >> and N495K) was inhibited by concentrations of [[ foscarnet ]] eight to 14 times higher than those required to inhibit wild-type polymerases.


The activity of polymerases containing mutations known to confer resistance to foscarnet (V715M, T700A and << N495K >>) was inhibited by concentrations of [[ foscarnet ]] eight to 14 times higher than those required to inhibit wild-type polymerases.


The activity of polymerases containing mutations known to confer resistance to foscarnet (V715M, T700A and N495K) was inhibited by concentrations of << foscarnet >> eight to 14 times higher than those required to inhibit wild-type [[ polymerases ]].


Absorption and secretion of << fluoride >> increase at acid pH levels, possibly because of its non-ionized state at these pHs and/or because of participation of a F(-)/H(+) cotransporter or a [[ F(-)/OH(-) antiporter ]].


Absorption and secretion of << fluoride >> increase at acid pH levels, possibly because of its non-ionized state at these pHs and/or because of participation of a [[ F(-)/H(+) cotransporter ]] or a F(-)/OH(-) antiporter.


Structure activity relationship studies of << tricyclic bispyran sulfone >> [[ γ-secretase ]] inhibitors.


An investigation is detailed of the structure activity relationships (SAR) of two sulfone side chains of compound (-)-1a (<< SCH 900229 >>), a potent, [[ PS1 ]]-selective γ-secretase inhibitor and clinical candidate for the treatment of Alzheimer's disease.


An investigation is detailed of the structure activity relationships (SAR) of two sulfone side chains of compound (-)-1a (<< SCH 900229 >>), a potent, PS1-selective [[ γ-secretase ]] inhibitor and clinical candidate for the treatment of Alzheimer's disease.


Culture of HepG2 cells with << griseofulvin >> has now been shown to induce both the formation of intracellular aggregates containing [[ K18 ]] as well as an increase in the abundance of K18 mRNA.


Culture of HepG2 cells with << griseofulvin >> has now been shown to induce both the formation of intracellular aggregates containing K18 as well as an increase in the abundance of [[ K18 ]] mRNA.


Low levels of << serotonin >> may reduce the density of the [[ serotonin transporter ]] (SERT) by either increasing trafficking or reducing synthesis; a "neuroadaptive response".


Low levels of << serotonin >> may reduce the density of the serotonin transporter ([[ SERT ]]) by either increasing trafficking or reducing synthesis; a "neuroadaptive response".


To determine whether << 3,4-methylenedioxymethamphetamine >> (MDMA)-induced reductions in [[ SERT ]] density could be related to such a mechanism, p-chlorophenylalanine or MDMA was administered to rats, and brain serotonin and SERT density were measured.


To determine whether 3,4-methylenedioxymethamphetamine (<< MDMA >>)-induced reductions in [[ SERT ]] density could be related to such a mechanism, p-chlorophenylalanine or MDMA was administered to rats, and brain serotonin and SERT density were measured.


However, only << MDMA >> reduced [[ SERT ]] density.


This observation suggests that << MDMA >>-induced reductions in [[ SERT ]] density do not represent neuroadaptive responses to decreased levels of brain serotonin, but may occur in response to some other stimulus or to the neurotoxic effects of MDMA.


<< Curcumin >> improves TNBS-induced colitis in rats by inhibiting [[ IL-27 ]] expression via the TLR4/NF-κB signaling pathway.


<< Curcumin >> improves TNBS-induced colitis in rats by inhibiting IL-27 expression via the [[ TLR4 ]]/NF-κB signaling pathway.


<< Curcumin >> improves TNBS-induced colitis in rats by inhibiting IL-27 expression via the TLR4/[[ NF-κB ]] signaling pathway.


This study explored whether << curcumin >> improves colonic inflammation in a rat colitis model through inhibition of the TLR4/NF-κB signaling pathway and [[ IL-27 ]] expression.


This study explored whether << curcumin >> improves colonic inflammation in a rat colitis model through inhibition of the [[ TLR4 ]]/NF-κB signaling pathway and IL-27 expression.


This study explored whether << curcumin >> improves colonic inflammation in a rat colitis model through inhibition of the TLR4/[[ NF-κB ]] signaling pathway and IL-27 expression.


Compared with the untreated colitis group, the << curcumin >>-treated group showed significant decreases in the disease activity index, colonic mucosa damage index, histological score, myeloperoxidase activity, and expressions of [[ NF-κB ]] mRNA, IL-27 mRNA, TLR4 protein, NF-κB p65 protein, and IL-27 p28 protein (p < 0.05).


Compared with the untreated colitis group, the << curcumin >>-treated group showed significant decreases in the disease activity index, colonic mucosa damage index, histological score, myeloperoxidase activity, and expressions of NF-κB mRNA, [[ IL-27 ]] mRNA, TLR4 protein, NF-κB p65 protein, and IL-27 p28 protein (p < 0.05).


Compared with the untreated colitis group, the << curcumin >>-treated group showed significant decreases in the disease activity index, colonic mucosa damage index, histological score, myeloperoxidase activity, and expressions of NF-κB mRNA, IL-27 mRNA, [[ TLR4 ]] protein, NF-κB p65 protein, and IL-27 p28 protein (p < 0.05).


Compared with the untreated colitis group, the << curcumin >>-treated group showed significant decreases in the disease activity index, colonic mucosa damage index, histological score, myeloperoxidase activity, and expressions of NF-κB mRNA, IL-27 mRNA, TLR4 protein, [[ NF-κB ]] p65 protein, and IL-27 p28 protein (p < 0.05).


Compared with the untreated colitis group, the << curcumin >>-treated group showed significant decreases in the disease activity index, colonic mucosa damage index, histological score, myeloperoxidase activity, and expressions of NF-κB mRNA, IL-27 mRNA, TLR4 protein, NF-κB [[ p65 ]] protein, and IL-27 p28 protein (p < 0.05).


Compared with the untreated colitis group, the << curcumin >>-treated group showed significant decreases in the disease activity index, colonic mucosa damage index, histological score, myeloperoxidase activity, and expressions of NF-κB mRNA, IL-27 mRNA, TLR4 protein, NF-κB p65 protein, and [[ IL-27 ]] p28 protein (p < 0.05).


Compared with the untreated colitis group, the << curcumin >>-treated group showed significant decreases in the disease activity index, colonic mucosa damage index, histological score, myeloperoxidase activity, and expressions of NF-κB mRNA, IL-27 mRNA, TLR4 protein, NF-κB p65 protein, and IL-27 [[ p28 ]] protein (p < 0.05).


Compared with the untreated colitis group, the << curcumin >>-treated group showed significant decreases in the disease activity index, colonic mucosa damage index, histological score, [[ myeloperoxidase ]] activity, and expressions of NF-κB mRNA, IL-27 mRNA, TLR4 protein, NF-κB p65 protein, and IL-27 p28 protein (p < 0.05).


There was no significant difference in << TLR4 >>, NF-κB, and IL-27 mRNA and proteins between [[ curcumin ]]-treated and sulfasalazine-treated groups.


There was no significant difference in TLR4, << NF-κB >>, and IL-27 mRNA and proteins between [[ curcumin ]]-treated and sulfasalazine-treated groups.


There was no significant difference in TLR4, NF-κB, and << IL-27 >> mRNA and proteins between [[ curcumin ]]-treated and sulfasalazine-treated groups.


There was no significant difference in << TLR4 >>, NF-κB, and IL-27 mRNA and proteins between curcumin-treated and [[ sulfasalazine ]]-treated groups.


There was no significant difference in TLR4, << NF-κB >>, and IL-27 mRNA and proteins between curcumin-treated and [[ sulfasalazine ]]-treated groups.


There was no significant difference in TLR4, NF-κB, and << IL-27 >> mRNA and proteins between curcumin-treated and [[ sulfasalazine ]]-treated groups.


The anti-inflammatory actions of << curcumin >> on colitis may involve inhibition of the TLR4/NF-κB signaling pathway and of [[ IL-27 ]] expression.


The anti-inflammatory actions of << curcumin >> on colitis may involve inhibition of the [[ TLR4 ]]/NF-κB signaling pathway and of IL-27 expression.


The anti-inflammatory actions of << curcumin >> on colitis may involve inhibition of the TLR4/[[ NF-κB ]] signaling pathway and of IL-27 expression.


A << KCC >> inhibitor-[[ [(dihydroindenyl)oxy] alkanoic acid ]] (DIOA)-blocked RVD more in HCEC than RCEC.


A << KCC >> inhibitor-[(dihydroindenyl)oxy] alkanoic acid ([[ DIOA ]])-blocked RVD more in HCEC than RCEC.


Under isotonic conditions, << N-ethylmaleimide >> (NEM) produced [[ KCC ]] activation and transient cell shrinkage.


Under isotonic conditions, N-ethylmaleimide (<< NEM >>) produced [[ KCC ]] activation and transient cell shrinkage.


Pharmacological properties of << lorglumide >> as a member of a new class of [[ cholecystokinin ]] antagonists.


Derivatives of << 5-(dipentylamino)-5-oxo-pentanoic acid >> are a new class of non-peptide cholecystokinin ([[ CCK ]]) antagonists.


Derivatives of << 5-(dipentylamino)-5-oxo-pentanoic acid >> are a new class of non-peptide [[ cholecystokinin ]] (CCK) antagonists.


The most potent compound, << D,L-4-(3,4-dichlorobenzoylamino)-5-(dipentylamino)-5-oxo-pen tanoic acid >> (lorglumide, CR 1409), has a great affinity for the pancreatic CCK receptors and is a competitive, specific and potent [[ CCK ]] antagonist on the smooth muscles of the gall bladder and ileum of the guinea pig and on the CCK-induced amylase secretion of isolated pancreatic acini.


The most potent compound, D,L-4-(3,4-dichlorobenzoylamino)-5-(dipentylamino)-5-oxo-pen tanoic acid (<< lorglumide >>, CR 1409), has a great affinity for the pancreatic CCK receptors and is a competitive, specific and potent [[ CCK ]] antagonist on the smooth muscles of the gall bladder and ileum of the guinea pig and on the CCK-induced amylase secretion of isolated pancreatic acini.


The most potent compound, D,L-4-(3,4-dichlorobenzoylamino)-5-(dipentylamino)-5-oxo-pen tanoic acid (lorglumide, << CR 1409 >>), has a great affinity for the pancreatic CCK receptors and is a competitive, specific and potent [[ CCK ]] antagonist on the smooth muscles of the gall bladder and ileum of the guinea pig and on the CCK-induced amylase secretion of isolated pancreatic acini.


In vivo << lorglumide >> antagonizes the contraction of the gall bladder of the guinea pig and of the dog provoked by i.v. [[ CCK-8 ]] or ceruletide (caerulein).


Synthesis and Structure-Activity Relationship Studies of Derivatives of the Dual << Aromatase >>-Sulfatase Inhibitor [[ 4-{[(4-Cyanophenyl)(4H-1,2,4-triazol-4-yl)amino]methyl}phenyl sulfamate ]].


Synthesis and Structure-Activity Relationship Studies of Derivatives of the Dual Aromatase-<< Sulfatase >> Inhibitor [[ 4-{[(4-Cyanophenyl)(4H-1,2,4-triazol-4-yl)amino]methyl}phenyl sulfamate ]].


4-{[(4-Cyanophenyl)(4H-1,2,4-triazol-4-yl)amino]methyl}phenyl sulfamate and its ortho-halogenated (<< F >>, Cl, Br) derivatives are first-generation dual [[ aromatase ]] and sulfatase inhibitors (DASIs).


4-{[(4-Cyanophenyl)(4H-1,2,4-triazol-4-yl)amino]methyl}phenyl sulfamate and its ortho-halogenated (<< F >>, Cl, Br) derivatives are first-generation dual aromatase and [[ sulfatase ]] inhibitors (DASIs).


<< 4-{[(4-Cyanophenyl)(4H-1,2,4-triazol-4-yl)amino]methyl}phenyl sulfamate >> and its ortho-halogenated (F, Cl, Br) derivatives are first-generation dual [[ aromatase ]] and sulfatase inhibitors (DASIs).


<< 4-{[(4-Cyanophenyl)(4H-1,2,4-triazol-4-yl)amino]methyl}phenyl sulfamate >> and its ortho-halogenated (F, Cl, Br) derivatives are first-generation dual aromatase and [[ sulfatase ]] inhibitors (DASIs).


4-{[(4-Cyanophenyl)(4H-1,2,4-triazol-4-yl)amino]methyl}phenyl sulfamate and its ortho-halogenated (F, << Cl >>, Br) derivatives are first-generation dual [[ aromatase ]] and sulfatase inhibitors (DASIs).


4-{[(4-Cyanophenyl)(4H-1,2,4-triazol-4-yl)amino]methyl}phenyl sulfamate and its ortho-halogenated (F, << Cl >>, Br) derivatives are first-generation dual aromatase and [[ sulfatase ]] inhibitors (DASIs).


4-{[(4-Cyanophenyl)(4H-1,2,4-triazol-4-yl)amino]methyl}phenyl sulfamate and its ortho-halogenated (F, Cl, << Br >>) derivatives are first-generation dual [[ aromatase ]] and sulfatase inhibitors (DASIs).


4-{[(4-Cyanophenyl)(4H-1,2,4-triazol-4-yl)amino]methyl}phenyl sulfamate and its ortho-halogenated (F, Cl, << Br >>) derivatives are first-generation dual aromatase and [[ sulfatase ]] inhibitors (DASIs).


The most potent in vitro DASI discovered is an << imidazole >> derivative with IC50 values against [[ aromatase ]] and steroid sulfatase in a JEG-3 cell preparation of 0.2 and 2.5 nM, respectively.


The most potent in vitro DASI discovered is an << imidazole >> derivative with IC50 values against aromatase and [[ steroid sulfatase ]] in a JEG-3 cell preparation of 0.2 and 2.5 nM, respectively.


The parent << phenol >> of this compound inhibits [[ aromatase ]] with an IC50 value of 0.028 nM in the same assay.


As revealed by glucose oxidase (GOD) and radioimmunoassay (RIA), both << dimethyldiguanide >> (DC, 0.6gkg(-1)d(-1)) and CPS (0.3, 0.6, 1.2gkg(-1)d(-1)) treatments significantly resulted in down-regulation of blood glucose and [[ insulin ]] levels in serum, while the levels of oxidative stress markers were markedly lowered through ELISA assay.


These findings demonstrate that cinnamon << polyphenols >> can exert the hypoglycemic and hypolipidemic effects through the mechanisms that may be associated with repairing pancreatic beta cells in diabetic mice and improving its anti-oxidative capacity, as well as attenuating cytotoxicity via inhibition of [[ iNOS ]], NF-κB activation.


These findings demonstrate that cinnamon << polyphenols >> can exert the hypoglycemic and hypolipidemic effects through the mechanisms that may be associated with repairing pancreatic beta cells in diabetic mice and improving its anti-oxidative capacity, as well as attenuating cytotoxicity via inhibition of iNOS, [[ NF-κB ]] activation.


These nonadrenoceptor binding sites may explain certain novel platelet aggregatory properties previously ascribed to << clonidine >> and endogenous clonidine-displacing substance(s), and may serve as markers of [[ imidazoline receptors ]] in humans.


Effects of << ORF 17583 >>, other [[ histamine H2-receptor ]] antagonists and omeprazole on gastric acid secretory states in rats and dogs.


<< ORF 17583 >>, a [[ histamine H2-receptor ]] antagonist, inhibited gastric acid secretion in pylorus-ligated rats (ED50 = 4.9 mg/kg intraduodenal; 3.4 mg/kg p.o.; and 0.21 mg/kg i.p.) and in total gastric fistula or Heidenhain pouch dogs stimulated by betazole (ED50 = 0.12 mg/kg p.o. and 0.08 mg/kg i.v.), histamine, tetragastrin, bethanechol, 2-deoxy-D-glucose or a meal (ED50 values ranged from 0.11-0.26 mg/kg p.o.).


This study examined the inward transport of << l-[(14)C]alanine >>, an [[ ASCT2 ]] preferential substrate, in monolayers of immortalized renal proximal tubular epithelial (PTE) cells from Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats.


In the presence of the system L inhibitor BCH, Na(+)-dependent l-alanine uptake in WKY and SHR PTE cells was inhibited by << alanine >>, serine, and cysteine, which is consistent with amino acid transport through [[ ASCT2 ]].


In the presence of the system L inhibitor BCH, Na(+)-dependent l-alanine uptake in WKY and SHR PTE cells was inhibited by alanine, << serine >>, and cysteine, which is consistent with amino acid transport through [[ ASCT2 ]].


In the presence of the system L inhibitor BCH, Na(+)-dependent l-alanine uptake in WKY and SHR PTE cells was inhibited by alanine, serine, and << cysteine >>, which is consistent with amino acid transport through [[ ASCT2 ]].


In the presence of the system L inhibitor BCH, Na(+)-dependent << l-alanine >> uptake in WKY and SHR PTE cells was inhibited by alanine, serine, and cysteine, which is consistent with amino acid transport through [[ ASCT2 ]].


In the presence of the system L inhibitor BCH, Na(+)-dependent l-alanine uptake in WKY and SHR PTE cells was inhibited by alanine, serine, and cysteine, which is consistent with << amino acid >> transport through [[ ASCT2 ]].


Differences in magnitude of << Na(+) >>-dependent l-alanine uptake through ASCT2 between WKY and SHR PTE cells correlated positively with differences in [[ ASCT2 ]] protein expression, this being more abundant in WKY PTE cells.


Differences in magnitude of Na(+)-dependent << l-alanine >> uptake through ASCT2 between WKY and SHR PTE cells correlated positively with differences in [[ ASCT2 ]] protein expression, this being more abundant in WKY PTE cells.


Differences in magnitude of Na(+)-dependent << l-alanine >> uptake through [[ ASCT2 ]] between WKY and SHR PTE cells correlated positively with differences in ASCT2 protein expression, this being more abundant in WKY PTE cells.


In conclusion, immortalized SHR and WKY PTE cells take up l-alanine mainly through a high-affinity << Na(+) >>-dependent amino acid transporter, with functional features of [[ ASCT2 ]] transport.


In conclusion, immortalized SHR and WKY PTE cells take up l-alanine mainly through a high-affinity Na(+)-dependent << amino acid >> transporter, with functional features of [[ ASCT2 ]] transport.


In conclusion, immortalized SHR and WKY PTE cells take up << l-alanine >> mainly through a high-affinity [[ Na(+)-dependent amino acid transporter ]], with functional features of ASCT2 transport.


In conclusion, immortalized SHR and WKY PTE cells take up << l-alanine >> mainly through a high-affinity Na(+)-dependent amino acid transporter, with functional features of [[ ASCT2 ]] transport.


The antipsychotic drugs << sertindole >> and pimozide block [[ erg3 ]], a human brain K(+) channel.


The antipsychotic drugs << sertindole >> and pimozide block erg3, a [[ human brain K(+) channel ]].


The antipsychotic drugs sertindole and << pimozide >> block [[ erg3 ]], a human brain K(+) channel.


The antipsychotic drugs sertindole and << pimozide >> block erg3, a [[ human brain K(+) channel ]].


The antipsychotic drugs << sertindole >> and pimozide are known to prolong the QT interval on the electrocardiogram via a high affinity block of the [[ cardiac K(+) channel ]] known as HERG (human ether-a-go-go-related gene; erg1).


The antipsychotic drugs << sertindole >> and pimozide are known to prolong the QT interval on the electrocardiogram via a high affinity block of the cardiac K(+) channel known as [[ HERG ]] (human ether-a-go-go-related gene; erg1).


The antipsychotic drugs << sertindole >> and pimozide are known to prolong the QT interval on the electrocardiogram via a high affinity block of the cardiac K(+) channel known as HERG ([[ human ether-a-go-go-related gene ]]; erg1).


The antipsychotic drugs << sertindole >> and pimozide are known to prolong the QT interval on the electrocardiogram via a high affinity block of the cardiac K(+) channel known as HERG (human ether-a-go-go-related gene; [[ erg1 ]]).


The antipsychotic drugs sertindole and << pimozide >> are known to prolong the QT interval on the electrocardiogram via a high affinity block of the [[ cardiac K(+) channel ]] known as HERG (human ether-a-go-go-related gene; erg1).


The antipsychotic drugs sertindole and << pimozide >> are known to prolong the QT interval on the electrocardiogram via a high affinity block of the cardiac K(+) channel known as [[ HERG ]] (human ether-a-go-go-related gene; erg1).


The antipsychotic drugs sertindole and << pimozide >> are known to prolong the QT interval on the electrocardiogram via a high affinity block of the cardiac K(+) channel known as HERG ([[ human ether-a-go-go-related gene ]]; erg1).


The antipsychotic drugs sertindole and << pimozide >> are known to prolong the QT interval on the electrocardiogram via a high affinity block of the cardiac K(+) channel known as HERG (human ether-a-go-go-related gene; [[ erg1 ]]).


Block of << erg3 >> by [[ sertindole ]] also displayed a positive voltage-dependence.


<< Pimozide >> blocked [[ erg3 ]] channel currents with an IC(50) of 103 nM and significant inhibition was noted at concentrations of 10 nM and higher.


We conclude that << erg3 >> can be blocked by certain antipsychotic drugs like [[ sertindole ]] and pimozide.


We conclude that << erg3 >> can be blocked by certain antipsychotic drugs like sertindole and [[ pimozide ]].


An amphiphile with branched << poly(ethylene glycol) >> architecture also activated the [[ lectin ]] pathway but only through L-ficolin recognition.


Conformational variations of both << phosphodiesterase-5 >> and inhibitors provide the structural basis for the physiological effects of vardenafil and [[ sildenafil ]].


<< Cucurbitacin I >> inhibits [[ rac1 ]] activation in breast cancer cells by a reactive oxygen species-mediated mechanism and independently of janus tyrosine kinase 2 and p-rex1.


Here we found that the anticancer agent << cucurbitacin I >>, a [[ Jak2 ]] inhibitor, reduced the activation of Rac1 and motility in response to the ErbB3 ligand heregulin in breast cancer cells.


Here we found that the anticancer agent << cucurbitacin I >>, a Jak2 inhibitor, reduced the activation of [[ Rac1 ]] and motility in response to the ErbB3 ligand heregulin in breast cancer cells.


Subsequent analysis revealed that << cucurbitacin I >> strongly activates [[ RhoA ]] and the Rho effector Rho kinase (ROCK) in breast cancer cells and induces the formation of stress fibers.


Subsequent analysis revealed that << cucurbitacin I >> strongly activates RhoA and the [[ Rho ]] effector Rho kinase (ROCK) in breast cancer cells and induces the formation of stress fibers.


Subsequent analysis revealed that << cucurbitacin I >> strongly activates RhoA and the Rho effector [[ Rho kinase ]] (ROCK) in breast cancer cells and induces the formation of stress fibers.


Subsequent analysis revealed that << cucurbitacin I >> strongly activates RhoA and the Rho effector Rho kinase ([[ ROCK ]]) in breast cancer cells and induces the formation of stress fibers.


Interestingly, disruption of the RhoA-ROCK pathway prevented the inhibitory effect of << cucurbitacin I >> on [[ Rac1 ]] activation by heregulin.


Lastly, we found that << RhoA >> activation by [[ cucurbitacin I ]] is mediated by reactive oxygen species (ROS).


The ROS scavenger << N-acetyl l-cysteine >> and the mitochondrial antioxidant Mito-TEMPO rescued the inhibitory effect of cucurbitacin I on [[ Rac1 ]] activation.


The ROS scavenger N-acetyl l-cysteine and the mitochondrial antioxidant Mito-TEMPO rescued the inhibitory effect of << cucurbitacin I >> on [[ Rac1 ]] activation.


Moreover, they established that the inhibitory effect of << cucurbitacin I >> on [[ Rac1 ]] activity involves the alteration of the balance between Rho and Rac.


Brain but not spinal << NR2B >> receptor is responsible for the anti-allodynic effect of an NR2B subunit-selective antagonist [[ CP-101,606 ]] in a rat chronic constriction injury model.


Brain but not spinal NR2B receptor is responsible for the anti-allodynic effect of an << NR2B >> subunit-selective antagonist [[ CP-101,606 ]] in a rat chronic constriction injury model.


In order to examine the site of action of an << NR2B >> subtype-selective NMDA antagonist [[ CP-101,606 ]], we investigated its analgesic effect in a rat model of neuropathic pain at various routes of administration.


In order to examine the site of action of an NR2B subtype-selective << NMDA >> antagonist [[ CP-101,606 ]], we investigated its analgesic effect in a rat model of neuropathic pain at various routes of administration.


These findings suggest that the anti-allodynia effect of << CP-101,606 >> is ascribable to blockade of [[ NR2B ]] receptors at the brain, but not at the spinal cord.


In contrast, intrathecal injection of a non-selective << NMDA >> antagonist, [[ memantine ]], significantly inhibited CCI-induced mechanical allodynia at a dose of 300 nmol, indicating the difference in the site of action between the non-selective NMDA antagonist and the NR2B-specific NMDA antagonist.


<< Rasagiline >> [N-propargyl-1R(+)-aminoindan; TVP1012] is a potent irreversible [[ monoamine oxidase ]] (MAO) inhibitor with selectivity for type B of the enzyme, which is being developed for treatment of Parkinson's disease.


<< Rasagiline >> [N-propargyl-1R(+)-aminoindan; TVP1012] is a potent irreversible monoamine oxidase ([[ MAO ]]) inhibitor with selectivity for type B of the enzyme, which is being developed for treatment of Parkinson's disease.


Rasagiline [N-propargyl-1R(+)-aminoindan; << TVP1012 >>] is a potent irreversible [[ monoamine oxidase ]] (MAO) inhibitor with selectivity for type B of the enzyme, which is being developed for treatment of Parkinson's disease.


Rasagiline [N-propargyl-1R(+)-aminoindan; << TVP1012 >>] is a potent irreversible monoamine oxidase ([[ MAO ]]) inhibitor with selectivity for type B of the enzyme, which is being developed for treatment of Parkinson's disease.


Rasagiline [<< N-propargyl-1R(+)-aminoindan >>; TVP1012] is a potent irreversible [[ monoamine oxidase ]] (MAO) inhibitor with selectivity for type B of the enzyme, which is being developed for treatment of Parkinson's disease.


Rasagiline [<< N-propargyl-1R(+)-aminoindan >>; TVP1012] is a potent irreversible monoamine oxidase ([[ MAO ]]) inhibitor with selectivity for type B of the enzyme, which is being developed for treatment of Parkinson's disease.


Reserpine-induced ptosis was reversed by << rasagiline >> at doses above 2 mg x kg(-1) i.p., which inhibit [[ MAO-A ]] as well as MAO-B, but not at MAO-B-selective doses.


Reserpine-induced ptosis was reversed by << rasagiline >> at doses above 2 mg x kg(-1) i.p., which inhibit MAO-A as well as [[ MAO-B ]], but not at MAO-B-selective doses.


However, combination of rasagiline (10 mg x kg(-1) i.p.) with L-DOPA or L-tryptophan (50 mg x kg(-1) i.p.), or rasagiline (10 mg x kg(-1) p.o.) with fluoxetine (10 mg x kg(-1) p.o.), did not induce the behavioural hyperactivity syndrome which is seen following inhibition of both << MAO-A >> and MAO-B by [[ tranylcypromine ]] together with the monoamine precursors.


However, combination of rasagiline (10 mg x kg(-1) i.p.) with L-DOPA or L-tryptophan (50 mg x kg(-1) i.p.), or rasagiline (10 mg x kg(-1) p.o.) with fluoxetine (10 mg x kg(-1) p.o.), did not induce the behavioural hyperactivity syndrome which is seen following inhibition of both MAO-A and << MAO-B >> by [[ tranylcypromine ]] together with the monoamine precursors.


However, combination of rasagiline (10 mg x kg(-1) i.p.) with L-DOPA or L-tryptophan (50 mg x kg(-1) i.p.), or rasagiline (10 mg x kg(-1) p.o.) with fluoxetine (10 mg x kg(-1) p.o.), did not induce the behavioural hyperactivity syndrome which is seen following inhibition of both << MAO-A >> and MAO-B by tranylcypromine together with the [[ monoamine ]] precursors.


However, combination of rasagiline (10 mg x kg(-1) i.p.) with L-DOPA or L-tryptophan (50 mg x kg(-1) i.p.), or rasagiline (10 mg x kg(-1) p.o.) with fluoxetine (10 mg x kg(-1) p.o.), did not induce the behavioural hyperactivity syndrome which is seen following inhibition of both MAO-A and << MAO-B >> by tranylcypromine together with the [[ monoamine ]] precursors.


<< Rasagiline >> does not modify CNS monoamine tissue levels or monoamine-induced behavioural syndromes at doses which selectively inhibit [[ MAO-B ]] but not MAO-A.


<< Rasagiline >> does not modify CNS monoamine tissue levels or monoamine-induced behavioural syndromes at doses which selectively inhibit MAO-B but not [[ MAO-A ]].


<< Omega class GSTs >> have dehydroascorbate reductase and thioltransferase activities and also catalyze the reduction of [[ monomethylarsonate ]], an intermediate in the pathway of arsenic biotransformation.


The latter reaction, catalyzed by << aspartoacylase >> (ASPA), produces [[ acetyl ]] groups plus aspartate and has been proposed to occur in both soluble and membranous subfractions of white matter.


The latter reaction, catalyzed by aspartoacylase (<< ASPA >>), produces [[ acetyl ]] groups plus aspartate and has been proposed to occur in both soluble and membranous subfractions of white matter.


The latter reaction, catalyzed by << aspartoacylase >> (ASPA), produces acetyl groups plus [[ aspartate ]] and has been proposed to occur in both soluble and membranous subfractions of white matter.


The latter reaction, catalyzed by aspartoacylase (<< ASPA >>), produces acetyl groups plus [[ aspartate ]] and has been proposed to occur in both soluble and membranous subfractions of white matter.


It is not yet clear whether << tamoxifen >> can reduce breast cancer incidence in women with BRCA1 and [[ BRCA2 ]] mutations, although preliminary evidence favors benefit for at least those with a BRCA2 mutation.


It is not yet clear whether << tamoxifen >> can reduce breast cancer incidence in women with BRCA1 and BRCA2 mutations, although preliminary evidence favors benefit for at least those with a [[ BRCA2 ]] mutation.


Troglitazone inhibited the antigen-induced production of LTB(4), C(4) and E(4) and the potency of the inhibition was comparable to that of << zileuton >>, a specific inhibitor of [[ 5-lipoxygenase ]] (5-LOX) and a clinically used anti-asthmatic drug.


Troglitazone inhibited the antigen-induced production of LTB(4), C(4) and E(4) and the potency of the inhibition was comparable to that of << zileuton >>, a specific inhibitor of 5-lipoxygenase ([[ 5-LOX ]]) and a clinically used anti-asthmatic drug.


Troglitazone inhibited LTB(4) production by the supernatant fraction of RBL-2H3 cell lysate with similar potency to << zileuton >>, suggesting that troglitazone inhibits LT production by direct inhibition of [[ 5-LOX ]] activity.


Troglitazone inhibited LTB(4) production by the supernatant fraction of RBL-2H3 cell lysate with similar potency to zileuton, suggesting that << troglitazone >> inhibits LT production by direct inhibition of [[ 5-LOX ]] activity.


These findings suggest that << troglitazone >> inhibits antigen-induced LT production in the IgE-sensitized RBL-2H3 cells and A23187-stimulated rat peritoneal neutrophils by direct inhibition of [[ 5-LOX ]] activity.


The positive correlation between << vitamin A >> and [[ immunoglobulin A ]] concentrations might be the result of the vitamin A inductive effect during immunoglobulins A synthesis.


The positive correlation between << vitamin A >> and immunoglobulin A concentrations might be the result of the vitamin A inductive effect during [[ immunoglobulins A ]] synthesis.


The positive correlation between vitamin A and << immunoglobulin A >> concentrations might be the result of the [[ vitamin A ]] inductive effect during immunoglobulins A synthesis.


The positive correlation between vitamin A and immunoglobulin A concentrations might be the result of the << vitamin A >> inductive effect during [[ immunoglobulins A ]] synthesis.


Experimental as well as clinical reports support the hypothesis that << calcium channel >> blockers such as [[ verapamil ]] may be an appropriate therapeutic approach in LQTS.


METHODS AND RESULTS: In 8 Langendorff-perfused rabbit hearts, << veratridine >> (0.1 microM), an inhibitor of [[ sodium channel ]] inactivation, led to a marked increase in QT-interval and simultaneously recorded monophasic ventricular action potentials (MAPs) (p < 0.05) thereby mimicking LQT3.


Specificity of << zebrafish retinol saturase >>: formation of [[ all-trans-13,14-dihydroretinol ]] and all-trans-7,8- dihydroretinol.


Specificity of << zebrafish retinol saturase >>: formation of all-trans-13,14-dihydroretinol and [[ all-trans-7,8- dihydroretinol ]].


Specifically, << all-trans-13,14-dihydroretinol >> is transiently oxidized to all-trans-13,14-dihydroretinoic acid before being oxidized further by [[ Cyp26 ]] enzymes.


Unlike mouse RetSat (mRetSat), << zRetSat A >> had an altered bond specificity saturating either the 13-14 or 7-8 double bonds of all-trans-retinol to produce either [[ all-trans-13,14-dihydroretinol ]] or all-trans-7,8-dihydroretinol, respectively.


Unlike mouse RetSat (mRetSat), << zRetSat A >> had an altered bond specificity saturating either the 13-14 or 7-8 double bonds of all-trans-retinol to produce either all-trans-13,14-dihydroretinol or [[ all-trans-7,8-dihydroretinol ]], respectively.


Unlike mouse RetSat (mRetSat), << zRetSat A >> had an altered bond specificity saturating either the 13-14 or 7-8 double bonds of [[ all-trans-retinol ]] to produce either all-trans-13,14-dihydroretinol or all-trans-7,8-dihydroretinol, respectively.


<< zRetSat A >> also saturated the 13-14 or 7-8 double bonds of [[ all-trans-3,4-didehydroretinol ]] (vitamin A2), a second endogenous form of vitamin A in zebrafish.


<< zRetSat A >> also saturated the 13-14 or 7-8 double bonds of all-trans-3,4-didehydroretinol ([[ vitamin A2 ]]), a second endogenous form of vitamin A in zebrafish.


<< Rasagiline >> is a novel, potent, and irreversible [[ monoamine oxidase type B ]] (MAO-B) inhibitor which has been approved for treatment of PD.


<< Rasagiline >> is a novel, potent, and irreversible monoamine oxidase type B ([[ MAO-B ]]) inhibitor which has been approved for treatment of PD.


<< Rasagiline >> inhibits [[ MAO-B ]] more potently than selegiline and has the advantage of once-daily dosing.


Analysis of splice variants and site-directed mutants of the AMPA receptor GluR3 expressed in Xenopus oocytes has shown that << lithium >> produces a large potentiation of the [[ GluR3 flop ]] splice variant and suggested that lithium might inhibit rapid desensitization, which is characteristic of this receptor (Karkanias, N. and Papke, R., Subtype-specific effects of lithium on glutamate receptor function. J. Neurophysiol., 81 (1999) 1506-1512).


Analysis of splice variants and site-directed mutants of the AMPA receptor GluR3 expressed in Xenopus oocytes has shown that lithium produces a large potentiation of the << GluR3 flop >> splice variant and suggested that [[ lithium ]] might inhibit rapid desensitization, which is characteristic of this receptor (Karkanias, N. and Papke, R., Subtype-specific effects of lithium on glutamate receptor function. J. Neurophysiol., 81 (1999) 1506-1512).


We now show that mutation of the 769R/ G desensitization site (Lomeli, H.M.J., Melcher, T., Hoger, T., Geiger, J.R., Kuner, T., Monyer, H., Higuchi, M.B.A. and Seeburg, P.H, Control of kinetic properties of AMPA receptor channels by nuclear RNA editing. Science, 9(266) (1994) 1709-1713) greatly attenuates the << lithium >>-induced potentiation of [[ GluR3 ]].


Additionally, experiments with the non-desensitizing site-directed mutant GluR3(L507Y) (Stern-Bach, Y., Russo, S., Neuman, M. and Rosenmund, C., A point mutation in the glutamate binding site blocks desensitization of AMPA receptors. Neuron, 21 (1998) 907-918) further confirms that << lithium >> enhances [[ GluR3 ]] responses by reducing desensitization, since lithium's effects are reversed in this mutant.


Specifically, << aniracetam >>, which potentiates wild-type [[ AMPA receptors ]], is ineffective on the non-desensitizing GluR3(L507Y) mutant, but has synergistic effects with lithium on wild-type receptors.


Specifically, aniracetam, which potentiates wild-type AMPA receptors, is ineffective on the non-desensitizing << GluR3 >>(L507Y) mutant, but has synergistic effects with [[ lithium ]] on wild-type receptors.


Specifically, aniracetam, which potentiates wild-type AMPA receptors, is ineffective on the non-desensitizing GluR3(<< L507Y >>) mutant, but has synergistic effects with [[ lithium ]] on wild-type receptors.


The << BH(4) >> treatment was associated with a 2-fold increase in [[ eNOS ]] activity as well as a 70% reduction in endothelial O(2)(-) production compared with those in fructose-fed rats.


The << BH(4) >> treatment also partially improved the [[ insulin ]] sensitivity and blood pressure, as well as the serum triglyceride concentration, in the fructose-fed rats.


Moreover, BH(4) treatment of the << fructose >>-fed rats markedly reduced the lipid peroxide content of both aortic and cardiac tissues and inhibited the activation of 2 redox-sensitive transcription factors, [[ nuclear factor-kappaB ]] and activating protein-1, which were increased in fructose-fed rats.


Moreover, BH(4) treatment of the << fructose >>-fed rats markedly reduced the lipid peroxide content of both aortic and cardiac tissues and inhibited the activation of 2 redox-sensitive transcription factors, nuclear factor-kappaB and [[ activating protein-1 ]], which were increased in fructose-fed rats.


Moreover, BH(4) treatment of the fructose-fed rats markedly reduced the lipid peroxide content of both aortic and cardiac tissues and inhibited the activation of 2 redox-sensitive transcription factors, << nuclear factor-kappaB >> and activating protein-1, which were increased in [[ fructose ]]-fed rats.


Moreover, BH(4) treatment of the fructose-fed rats markedly reduced the lipid peroxide content of both aortic and cardiac tissues and inhibited the activation of 2 redox-sensitive transcription factors, nuclear factor-kappaB and << activating protein-1 >>, which were increased in [[ fructose ]]-fed rats.


Moreover, << BH(4) >> treatment of the fructose-fed rats markedly reduced the lipid peroxide content of both aortic and cardiac tissues and inhibited the activation of 2 redox-sensitive transcription factors, [[ nuclear factor-kappaB ]] and activating protein-1, which were increased in fructose-fed rats.


Moreover, << BH(4) >> treatment of the fructose-fed rats markedly reduced the lipid peroxide content of both aortic and cardiac tissues and inhibited the activation of 2 redox-sensitive transcription factors, nuclear factor-kappaB and [[ activating protein-1 ]], which were increased in fructose-fed rats.


It has been claimed that << hCTR1 >>, the human high affinity copper transporter, is the major entry pathway for [[ cDDP ]] and related drugs via a mechanism that mimics copper.


It has been claimed that hCTR1, the << human high affinity copper transporter >>, is the major entry pathway for [[ cDDP ]] and related drugs via a mechanism that mimics copper.


We confirm the correlation between higher << hCTR1 >> levels and higher [[ Pt ]]-drug uptake in tumor cells sensitive to the drug.


In the DRN, << brexpiprazole >> completely inhibited the firing of 5-HT neurons via [[ 5-HT1A ]] agonism and was more potent than aripiprazole (ED50 = 230 and 700 mug/kg, respectively).


In the DRN, brexpiprazole completely inhibited the firing of 5-HT neurons via << 5-HT1A >> agonism and was more potent than [[ aripiprazole ]] (ED50 = 230 and 700 mug/kg, respectively).


In the locus coeruleus, brexpiprazole reversed the inhibitory effect of the preferential << 5-HT2A >> receptor agonist [[ DOI ]] (2,5-dimethoxy-4-iodoamphetamine) on norepinephrine neuronal firing (ED50 = 110 mug/kg), demonstrating 5-HT2A antagonistic action.


In the locus coeruleus, brexpiprazole reversed the inhibitory effect of the preferential << 5-HT2A >> receptor agonist DOI ([[ 2,5-dimethoxy-4-iodoamphetamine ]]) on norepinephrine neuronal firing (ED50 = 110 mug/kg), demonstrating 5-HT2A antagonistic action.


Brexpiprazole reversed the inhibitory effect of the DA agonist << apomorphine >> on VTA DA neurons (ED50 = 61 mug/kg), whereas it was ineffective when administered alone, indicating partial agonistic action on [[ D2 receptors ]].


Compared with aripiprazole, which significantly inhibited the firing activity of VTA DA neurons, << brexpiprazole >> displayed less efficacy at [[ D2 receptors ]].


In the hippocampus, << brexpiprazole >> acted as a full agonist at [[ 5-HT1A ]] receptors on pyramidal neurons.


In the lateral geniculate nucleus, << brexpiprazole >> displayed [[ alpha1B-adrenoceptor ]] antagonistic action.


For << AII >> and ET1, MAP was also increased for the [[ fenofibrate ]] group but not in a dose-dependent fashion.


For AII and << ET1 >>, MAP was also increased for the [[ fenofibrate ]] group but not in a dose-dependent fashion.


Nanobody-albumin nanoparticles (NANAPs) for the delivery of a << multikinase >> inhibitor [[ 17864 ]] to EGFR overexpressing tumor cells.


Glutaraldehyde crosslinked albumin nanoparticles with a size of approximately 100nm were loaded with the << multikinase >> inhibitor [[ 17864 ]]-L(x)-a platinum-bound sunitinib analogue-which couples the drug to methionine residues of albumin and is released in a reductive environment.


Endogenously produced asymmetrically methylated << arginine >> residues are competitive inhibitors of all three isoforms of [[ nitric oxide synthase ]] (NOS).


Endogenously produced asymmetrically methylated << arginine >> residues are competitive inhibitors of all three isoforms of nitric oxide synthase ([[ NOS ]]).


The enzyme << dimethylarginine dimethylaminohydrolase >> (DDAH) specifically hydrolyzes these asymmetrically methylated [[ arginine ]] residues to citrulline and methylamines.


The enzyme dimethylarginine dimethylaminohydrolase (<< DDAH >>) specifically hydrolyzes these asymmetrically methylated [[ arginine ]] residues to citrulline and methylamines.


Previously we have proposed that regulation of asymmetric << methylarginine >> concentration by [[ DDAH ]] may provide a novel mechanism for the regulation of NOS activity in vivo.


Structure-based design of novel << dihydroisoquinoline >> [[ BACE-1 ]] inhibitors that do not engage the catalytic aspartates.


The structure-activity relationship of a series of << dihydroisoquinoline >> [[ BACE-1 ]] inhibitors is described.


Tissue-type plasminogen activator (tPA), a << serine >> protease well known for generating plasmin, has been demonstrated to induce [[ matrix metalloproteinase-9 ]] (MMP-9) gene expression and protein secretion in renal interstitial fibroblasts.


Tissue-type plasminogen activator (tPA), a << serine >> protease well known for generating [[ plasmin ]], has been demonstrated to induce matrix metalloproteinase-9 (MMP-9) gene expression and protein secretion in renal interstitial fibroblasts.


Furthermore, tPA induced rapid << tyrosine >> phosphorylation on the beta subunit of LRP-1, which was followed by the activation of [[ Mek1 ]] and its downstream Erk-1 and -2.


Furthermore, tPA induced rapid << tyrosine >> phosphorylation on the beta subunit of LRP-1, which was followed by the activation of Mek1 and its downstream [[ Erk-1 and -2 ]].


The data show that << CP[c]Ph >> is less potent at inducing [[ CYP1A ]] gene expression in rainbow trout than benzo[a]pyrene (B[a]P), a well-known Ah-receptor agonist.


The data show that CP[c]Ph is less potent at inducing << CYP1A >> gene expression in rainbow trout than [[ benzo[a]pyrene ]] (B[a]P), a well-known Ah-receptor agonist.


The data show that CP[c]Ph is less potent at inducing << CYP1A >> gene expression in rainbow trout than benzo[a]pyrene ([[ B[a]P ]]), a well-known Ah-receptor agonist.


Interestingly, the << CP[c]Ph >> dependent up-regulation of [[ CYP1A ]] mRNA is positively correlated with the incidences of clastogenic changes in rainbow trout erythrocytes.


<< CP[c]Ph >> has, comparably to B[a]P, a potential to repress expression of [[ tumor suppressor p53 ]], in the head kidney of rainbow trout.


CP[c]Ph has, comparably to << B[a]P >>, a potential to repress expression of [[ tumor suppressor p53 ]], in the head kidney of rainbow trout.


Identification of << benzofuran >> central cores for the inhibition of [[ leukotriene A(4) hydrolase ]].


Leukotriene A(4) hydrolase (<< LTA(4)H >>) is a cystolic enzyme that stereospecifically catalyzes the transformation of LTA(4) to [[ LTB(4) ]].


<< Leukotriene A(4) hydrolase >> (LTA(4)H) is a cystolic enzyme that stereospecifically catalyzes the transformation of LTA(4) to [[ LTB(4) ]].


Leukotriene A(4) hydrolase (<< LTA(4)H >>) is a cystolic enzyme that stereospecifically catalyzes the transformation of [[ LTA(4) ]] to LTB(4).


<< Leukotriene A(4) hydrolase >> (LTA(4)H) is a cystolic enzyme that stereospecifically catalyzes the transformation of [[ LTA(4) ]] to LTB(4).


This paper describes the identification and synthesis of substituted << benzofurans >> as [[ LTH(4)H ]] inhibitors.


<< Benzofuran >> 28 showed dose responsive target engagement and provides a useful tool to explore a [[ LTA(4)H ]] inhibitor for the treatment of inflammatory diseases, such as asthma and inflammatory bowel disease (IBD).


<< Minocycline >> treatment prevents the formation of activated [[ caspase-3 ]], a known effector of apoptosis, as well as the appearance of a calpain cleaved substrate, a marker of excitotoxic/necrotic cell death.


Neurochemical effects of the << monoamine oxidase >> inhibitor [[ phenelzine ]] on brain GABA and alanine: A comparison with vigabatrin.


PURPOSE: To compare << phenelzine >> (PLZ), an antidepressant drug with anxiolytic properties which inhibits [[ monoamine oxidase ]] (MAO) but also elevates rat brain levels of the amino acids ?-aminobutyric acid (GABA) and alanine (ALA), with vigabatrin (VIG), an anticonvulsant which elevates brain GABA by inhibition of GABA transaminase (GABA-T), with regard to their actions on brain levels of GABA and ALA and on activities of MAO, GABA-T and ALA transaminase (ALA-T).


PURPOSE: To compare << phenelzine >> (PLZ), an antidepressant drug with anxiolytic properties which inhibits monoamine oxidase ([[ MAO ]]) but also elevates rat brain levels of the amino acids ?-aminobutyric acid (GABA) and alanine (ALA), with vigabatrin (VIG), an anticonvulsant which elevates brain GABA by inhibition of GABA transaminase (GABA-T), with regard to their actions on brain levels of GABA and ALA and on activities of MAO, GABA-T and ALA transaminase (ALA-T).


PURPOSE: To compare phenelzine (PLZ), an antidepressant drug with anxiolytic properties which inhibits monoamine oxidase (MAO) but also elevates rat brain levels of the amino acids ?-aminobutyric acid (GABA) and alanine (ALA), with << vigabatrin >> (VIG), an anticonvulsant which elevates brain GABA by inhibition of [[ GABA transaminase ]] (GABA-T), with regard to their actions on brain levels of GABA and ALA and on activities of MAO, GABA-T and ALA transaminase (ALA-T).