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Cells were also evaluated in the presence of << wortmannin >>, an inhibitor of phosphatidylinositol 3-kinases and thus [[ AKt ]] (0-100 nM).

Cells were also evaluated in the presence of << wortmannin >>, an inhibitor of [[ phosphatidylinositol 3-kinases ]] and thus AKt (0-100 nM).

Saturated << palmitic and stearic acids >> increased ceramides, up-regulated PTP1B, and had AKt and [[ PTP1B ]] phosphorylation at Ser 50 impaired.

Saturated << palmitic and stearic acids >> increased ceramides, up-regulated PTP1B, and had [[ AKt ]] and PTP1B phosphorylation at Ser 50 impaired.

Saturated << palmitic and stearic acids >> increased ceramides, up-regulated [[ PTP1B ]], and had AKt and PTP1B phosphorylation at Ser 50 impaired.

Only FFAs that increased << ceramides >> caused impairment of [[ AKt ]] and PTP1B phosphorylation at Ser 50.

Only FFAs that increased << ceramides >> caused impairment of AKt and [[ PTP1B ]] phosphorylation at Ser 50.

Indoleamine 2,3-dioxygenase (<< IDO >>), a [[ tryptophan ]] catabolizing enzyme, has been implicated in the pathogenesis of various neurological disorders.

<< Indoleamine 2,3-dioxygenase >> (IDO), a [[ tryptophan ]] catabolizing enzyme, has been implicated in the pathogenesis of various neurological disorders.

To determine whether dysregulation of SIRT1 promotes NADPH oxidase-dependent production of reactive oxygen species (ROS) and impairs endothelial function we assessed the effects of three structurally different inhibitors of << SIRT1 >> ([[ nicotinamide ]], sirtinol, EX527) in aorta segments isolated from young Wistar rats.

To determine whether dysregulation of SIRT1 promotes NADPH oxidase-dependent production of reactive oxygen species (ROS) and impairs endothelial function we assessed the effects of three structurally different inhibitors of << SIRT1 >> (nicotinamide, [[ sirtinol ]], EX527) in aorta segments isolated from young Wistar rats.

To determine whether dysregulation of SIRT1 promotes NADPH oxidase-dependent production of reactive oxygen species (ROS) and impairs endothelial function we assessed the effects of three structurally different inhibitors of << SIRT1 >> (nicotinamide, sirtinol, [[ EX527 ]]) in aorta segments isolated from young Wistar rats.

To determine whether dysregulation of SIRT1 promotes << NADPH oxidase >>-dependent production of reactive [[ oxygen ]] species (ROS) and impairs endothelial function we assessed the effects of three structurally different inhibitors of SIRT1 (nicotinamide, sirtinol, EX527) in aorta segments isolated from young Wistar rats.

Endothelial dysfunction induced by SIRT1 inhibition was prevented by treatment of the vessels with the << NADPH oxidase >> inhibitor [[ apocynin ]] or superoxide dismutase.

Inhibition of SIRT1 significantly increased vascular superoxide production, enhanced << NADPH oxidase >> activity, and mRNA expression of its subunits p22(phox) and NOX4, which were prevented by [[ resveratrol ]].

Inhibition of SIRT1 significantly increased vascular superoxide production, enhanced NADPH oxidase activity, and mRNA expression of its subunits << p22(phox) >> and NOX4, which were prevented by [[ resveratrol ]].

Inhibition of SIRT1 significantly increased vascular superoxide production, enhanced NADPH oxidase activity, and mRNA expression of its subunits p22(phox) and << NOX4 >>, which were prevented by [[ resveratrol ]].

Inhibition of SIRT1 significantly increased vascular superoxide production, enhanced << NADPH oxidase >> activity, and mRNA expression of its subunits p22(phox) and NOX4, which were prevented by [[ resveratrol ]].

Inhibition of SIRT1 significantly increased vascular superoxide production, enhanced NADPH oxidase activity, and mRNA expression of its subunits << p22(phox) >> and NOX4, which were prevented by [[ resveratrol ]].

Inhibition of SIRT1 significantly increased vascular superoxide production, enhanced NADPH oxidase activity, and mRNA expression of its subunits p22(phox) and << NOX4 >>, which were prevented by [[ resveratrol ]].

Inhibition of << SIRT1 >> significantly increased vascular [[ superoxide ]] production, enhanced NADPH oxidase activity, and mRNA expression of its subunits p22(phox) and NOX4, which were prevented by resveratrol.

Peroxisome proliferator-activated receptor-α (PPARα) activation mimicked the effects of << resveratrol >> while PPARα inhibition prevented the effects of this [[ SIRT1 ]] activator.

SIRT1 co-precipitated with PPARα and << nicotinamide >> increased the acetylation of the PPARα coactivator [[ PGC-1α ]], which was suppressed by resveratrol.

SIRT1 co-precipitated with PPARα and nicotinamide increased the acetylation of the PPARα coactivator << PGC-1α >>, which was suppressed by [[ resveratrol ]].

<< EROD >> activity induction in peripheral blood lymphocytes, liver and brain tissues of rats orally exposed to [[ polycyclic aromatic hydrocarbons ]].

Little is known in terms of multi-matrix << cytochrome P450 >> activity induction under repeated oral exposure to planar [[ halogenated and polycyclic aromatic hydrocarbons ]] (PHH, PAH).

Little is known in terms of multi-matrix << cytochrome P450 >> activity induction under repeated oral exposure to planar halogenated and polycyclic aromatic hydrocarbons (PHH, [[ PAH ]]).

Repression of farnesyltransferase (FNTA) by siRNA and the enzyme inhibitor << manumycin A >> caused elevation of [[ ApoA-I ]] secretion from hepatocytes and from transgenic mice expressing hApoA-I and cholesterol ester transfer protein transgenes.

Repression of farnesyltransferase (FNTA) by siRNA and the enzyme inhibitor << manumycin A >> caused elevation of ApoA-I secretion from hepatocytes and from transgenic mice expressing [[ hApoA-I ]] and cholesterol ester transfer protein transgenes.

Repression of << farnesyltransferase >> (FNTA) by siRNA and the enzyme inhibitor [[ manumycin A ]] caused elevation of ApoA-I secretion from hepatocytes and from transgenic mice expressing hApoA-I and cholesterol ester transfer protein transgenes.

Repression of farnesyltransferase (<< FNTA >>) by siRNA and the enzyme inhibitor [[ manumycin A ]] caused elevation of ApoA-I secretion from hepatocytes and from transgenic mice expressing hApoA-I and cholesterol ester transfer protein transgenes.

<< Estrogens >> are biosynthesised from androgens by the [[ CYP450 ]] enzyme complex called aromatase.

<< Estrogens >> are biosynthesised from androgens by the CYP450 enzyme complex called [[ aromatase ]].

Estrogens are biosynthesised from << androgens >> by the CYP450 enzyme complex called [[ aromatase ]].

In breast cancer, intratumoural << aromatase >> is the source for local [[ estrogen ]] production in the tissue.

The potent and selective third-generation << aromatase >> inhibitors anastrozole, [[ letrozole ]] and exemestane were introduced to the market as endocrine therapy in postmenopausal patients failing anti-estrogen therapy alone, or multiple hormonal therapies.

The potent and selective third-generation << aromatase >> inhibitors [[ anastrozole ]], letrozole and exemestane were introduced to the market as endocrine therapy in postmenopausal patients failing anti-estrogen therapy alone, or multiple hormonal therapies.

<< Anastrozole >> and letrozole are both non-steroidal [[ aromatase ]] inhibitors that compete with the substrate for binding to the enzyme active site.

Anastrozole and << letrozole >> are both non-steroidal [[ aromatase ]] inhibitors that compete with the substrate for binding to the enzyme active site.

Identification and synthesis of << N-(thiophen-2-yl) benzamide >> derivatives as [[ BRAF ]](V600E) inhibitors.

Identification and synthesis of << N-(thiophen-2-yl) benzamide >> derivatives as BRAF([[ V600E ]]) inhibitors.

In this study, we employed virtual screening and chemical synthesis to identify a series of << N-(thiophen-2-yl) benzamide >> derivatives as potent [[ BRAF ]](V600E) inhibitors.

In this study, we employed virtual screening and chemical synthesis to identify a series of << N-(thiophen-2-yl) benzamide >> derivatives as potent BRAF([[ V600E ]]) inhibitors.

Exposure of cells to 4mM << NaF >> for 24h induced [[ caspase-3 ]] activation, ultrastructural alterations, and resulted in the translocation of Bax to the mitochondria and the release of cytochrome c from the mitochondrial inter-membrane space into the cytosol, indicating that fluoride-mediated apoptosis is mitochondria-dependent.

<< Fluoride >> treatment also increased phosphorylation of [[ JNK ]] and ERK, but not p38, and apoptosis induced by fluoride was notably or partly suppressed by treatment with JNK or ERK inhibitors, respectively.

<< Fluoride >> treatment also increased phosphorylation of JNK and [[ ERK ]], but not p38, and apoptosis induced by fluoride was notably or partly suppressed by treatment with JNK or ERK inhibitors, respectively.

Furthermore, the << Panx1 >> channel blockers [[ carbenoxolone ]] and Probenecid were less effective in inhibiting Panx1 currents when Kvbeta3 was co-expressed.

Furthermore, the << Panx1 >> channel blockers carbenoxolone and [[ Probenecid ]] were less effective in inhibiting Panx1 currents when Kvbeta3 was co-expressed.

<< (-)-6-(7-Methoxy-2-(trifluoromethyl)pyrazolo[1,5-a]pyridin-4-yl)-5-methyl-4,5-dihydropyridazin-3(2H)-one >> (KCA-1490) exhibits moderate dual [[ PDE3/4 ]]-inhibitory activity and promises as a combined bronchodilatory/anti-inflammatory agent.

(-)-6-(7-Methoxy-2-(trifluoromethyl)pyrazolo[1,5-a]pyridin-4-yl)-5-methyl-4,5-dihydropyridazin-3(2H)-one (<< KCA-1490 >>) exhibits moderate dual [[ PDE3/4 ]]-inhibitory activity and promises as a combined bronchodilatory/anti-inflammatory agent.

<< N >>-alkylation of the pyridazinone ring markedly enhances potency against [[ PDE4 ]] but suppresses PDE3 inhibition.

<< N >>-alkylation of the pyridazinone ring markedly enhances potency against PDE4 but suppresses [[ PDE3 ]] inhibition.

N-alkylation of the << pyridazinone >> ring markedly enhances potency against [[ PDE4 ]] but suppresses PDE3 inhibition.

N-alkylation of the << pyridazinone >> ring markedly enhances potency against PDE4 but suppresses [[ PDE3 ]] inhibition.

Addition of a << 6-aryl-4,5-dihydropyridazin-3(2H)-one >> extension to the N-alkyl group facilitates both enhancement of [[ PDE4 ]]-inhibitory activity and restoration of potent PDE3 inhibition.

Addition of a << 6-aryl-4,5-dihydropyridazin-3(2H)-one >> extension to the N-alkyl group facilitates both enhancement of PDE4-inhibitory activity and restoration of potent [[ PDE3 ]] inhibition.

Addition of a 6-aryl-4,5-dihydropyridazin-3(2H)-one extension to the << N >>-alkyl group facilitates both enhancement of [[ PDE4 ]]-inhibitory activity and restoration of potent PDE3 inhibition.

Addition of a 6-aryl-4,5-dihydropyridazin-3(2H)-one extension to the << N >>-alkyl group facilitates both enhancement of PDE4-inhibitory activity and restoration of potent [[ PDE3 ]] inhibition.

Fumarate reductase (<< FRD >>) is the key enzyme in [[ fumarate ]] respiration induced by anaerobic growth of bacteria.

<< Fumarate reductase >> (FRD) is the key enzyme in [[ fumarate ]] respiration induced by anaerobic growth of bacteria.

The frdA gene coding for subunit A of FRD, and two control genes, << copA >> and copP associated with the export of [[ copper ]] out of H. pylori, were inactivated by insertion of the chloramphenicol acetyltransferase cassette into these individual genes.

The frdA gene coding for subunit A of FRD, and two control genes, copA and << copP >> associated with the export of [[ copper ]] out of H. pylori, were inactivated by insertion of the chloramphenicol acetyltransferase cassette into these individual genes.

Given that << FRD >>, present in all H. pylori strains, is immunogenic in H. pylori -infected patients and H. pylori growth in vitro can be inhibited by three anthelmintics ([[ morantel ]], oxantel and thiabendazole), this enzyme could potentially be used both as a novel drug target as well as in the development of vaccines for H. pylori prevention and eradication.

Given that << FRD >>, present in all H. pylori strains, is immunogenic in H. pylori -infected patients and H. pylori growth in vitro can be inhibited by three anthelmintics (morantel, [[ oxantel ]] and thiabendazole), this enzyme could potentially be used both as a novel drug target as well as in the development of vaccines for H. pylori prevention and eradication.

Given that << FRD >>, present in all H. pylori strains, is immunogenic in H. pylori -infected patients and H. pylori growth in vitro can be inhibited by three anthelmintics (morantel, oxantel and [[ thiabendazole ]]), this enzyme could potentially be used both as a novel drug target as well as in the development of vaccines for H. pylori prevention and eradication.

To begin to examine whether these changes are mediated by alterations in gene expression for << tryptophan hydroxylase >> (TPH), the rate-limiting enzyme in [[ 5-HT ]] biosynthesis, we quantitated its mRNA levels by competitive reverse transcription-polymerase chain reaction (RT-PCR).

To begin to examine whether these changes are mediated by alterations in gene expression for tryptophan hydroxylase (<< TPH >>), the rate-limiting enzyme in [[ 5-HT ]] biosynthesis, we quantitated its mRNA levels by competitive reverse transcription-polymerase chain reaction (RT-PCR).

In contrast, there was little change in mRNA levels for << GTP cyclohydrolase I >> (GTPCH), the rate limiting enzyme in synthesis of the [[ tetrahydrobiopterin ]] (BH4), the obligate cofactor for TPH.

In contrast, there was little change in mRNA levels for GTP cyclohydrolase I (<< GTPCH >>), the rate limiting enzyme in synthesis of the [[ tetrahydrobiopterin ]] (BH4), the obligate cofactor for TPH.

In contrast, there was little change in mRNA levels for << GTP cyclohydrolase I >> (GTPCH), the rate limiting enzyme in synthesis of the tetrahydrobiopterin ([[ BH4 ]]), the obligate cofactor for TPH.

In contrast, there was little change in mRNA levels for GTP cyclohydrolase I (<< GTPCH >>), the rate limiting enzyme in synthesis of the tetrahydrobiopterin ([[ BH4 ]]), the obligate cofactor for TPH.

In relation to zinc bioavailability, << α-CPPs >>, β-CPPs, α(s1)-CN(64-74)4P and β-CN(1-25)4P increased [[ zinc ]] uptake.

In relation to zinc bioavailability, α-CPPs, << β-CPPs >>, α(s1)-CN(64-74)4P and β-CN(1-25)4P increased [[ zinc ]] uptake.

In relation to zinc bioavailability, α-CPPs, β-CPPs, << α(s1)-CN >>(64-74)4P and β-CN(1-25)4P increased [[ zinc ]] uptake.

In relation to zinc bioavailability, α-CPPs, β-CPPs, α(s1)-CN(64-74)4P and << β-CN >>(1-25)4P increased [[ zinc ]] uptake.

In contrast to parenteral delivery of rBChE, which currently requires posttranslational modification for good plasma stability, an unmodified aer-rBChE pretreatment given 1-40h prior to >1 LD50 of aer-<< paraoxon >> (Px) was able to prevent inhibition of circulating [[ cholinesterase ]] in a dose-dependent manner.

Next to << Glut-4 >>, the predominant protein influencing [[ glucose ]] metabolism is PPARα and γ whose expressions were also positively modulated.

Both the << 5 alpha-reductase >> inhibitor [[ finasteride ]] and alpha 1-adrenoceptor antagonists (e.g. alfuzosin, doxazosin, prazosin, tamsulosin and terazosin) have been recommended as appropriate treatment options for patients with lower urinary tract symptoms (LUTS) associated with benign prostatic obstruction (BPO), and their efficacy has been proven in several placebo-controlled trials.

Both the 5 alpha-reductase inhibitor finasteride and << alpha 1-adrenoceptor >> antagonists (e.g. [[ alfuzosin ]], doxazosin, prazosin, tamsulosin and terazosin) have been recommended as appropriate treatment options for patients with lower urinary tract symptoms (LUTS) associated with benign prostatic obstruction (BPO), and their efficacy has been proven in several placebo-controlled trials.

Both the 5 alpha-reductase inhibitor finasteride and << alpha 1-adrenoceptor >> antagonists (e.g. alfuzosin, [[ doxazosin ]], prazosin, tamsulosin and terazosin) have been recommended as appropriate treatment options for patients with lower urinary tract symptoms (LUTS) associated with benign prostatic obstruction (BPO), and their efficacy has been proven in several placebo-controlled trials.

Both the 5 alpha-reductase inhibitor finasteride and << alpha 1-adrenoceptor >> antagonists (e.g. alfuzosin, doxazosin, [[ prazosin ]], tamsulosin and terazosin) have been recommended as appropriate treatment options for patients with lower urinary tract symptoms (LUTS) associated with benign prostatic obstruction (BPO), and their efficacy has been proven in several placebo-controlled trials.

Both the 5 alpha-reductase inhibitor finasteride and << alpha 1-adrenoceptor >> antagonists (e.g. alfuzosin, doxazosin, prazosin, [[ tamsulosin ]] and terazosin) have been recommended as appropriate treatment options for patients with lower urinary tract symptoms (LUTS) associated with benign prostatic obstruction (BPO), and their efficacy has been proven in several placebo-controlled trials.

Both the 5 alpha-reductase inhibitor finasteride and << alpha 1-adrenoceptor >> antagonists (e.g. alfuzosin, doxazosin, prazosin, tamsulosin and [[ terazosin ]]) have been recommended as appropriate treatment options for patients with lower urinary tract symptoms (LUTS) associated with benign prostatic obstruction (BPO), and their efficacy has been proven in several placebo-controlled trials.

Central << 5-HT3 >> receptor stimulation by [[ m-CPBG ]] increases blood glucose in rats.

Injections of << m-CPBG >>, a selective [[ 5-HT3 ]] receptor agonist, induced a significant increase in blood glucose in non-stressed rats in both fasted and in fed states.

The hyperglycemic effect of << m-CPBG >> central administration was blocked by pretreatment with ondansetron, a specific [[ 5-HT3 ]] receptor antagonist, indicating that the effects here obtained with m-CPBG were a result of its interaction with 5-HT3 receptors.

<< 3'-R/S-Hydroxyvoacamine >>, a potent [[ acetylcholinesterase ]] inhibitor from Tabernaemontana divaricata.

Guided by the << acetylcholinesterase >> inhibiting activity, the [[ bisindole alkaloid ]] 3'-R/S-hydroxyvoacamine was isolated from a stem extract of Tabernaemontana divaricata, a plant used in Thailand in traditional rejuvenation remedies for improving the memory.

Guided by the << acetylcholinesterase >> inhibiting activity, the bisindole alkaloid [[ 3'-R/S-hydroxyvoacamine ]] was isolated from a stem extract of Tabernaemontana divaricata, a plant used in Thailand in traditional rejuvenation remedies for improving the memory.

<< α-Amino-α´-Halomethylketones >>: Synthetic Methodologies and Pharmaceutical Applications as [[ Serine and Cysteine Protease ]] Inhibitors.

Introduction: 5-Lipoxygenase (<< 5-LO >>) is a crucial enzyme of the [[ arachidonic acid ]] (AA) cascade and catalyzes the formation of bioactive leukotrienes (LTs) with the help of FLAP, the 5-LO-activating protein.

Introduction: << 5-Lipoxygenase >> (5-LO) is a crucial enzyme of the [[ arachidonic acid ]] (AA) cascade and catalyzes the formation of bioactive leukotrienes (LTs) with the help of FLAP, the 5-LO-activating protein.

Using a transient heterologous cell expression system, we find that the transport activities of the << short OATP2B1 >> variant towards substrates [[ estrone sulfate ]] and rosuvastatin are similar to the well-characterized full length variant.

Using a transient heterologous cell expression system, we find that the transport activities of the << short OATP2B1 >> variant towards substrates estrone sulfate and [[ rosuvastatin ]] are similar to the well-characterized full length variant.

<< Memantine >> is an uncompetitive (channel blocking) [[ NMDA receptor ]] antagonist.

Like other << NMDA receptor >> antagonists, [[ memantine ]] at high concentrations can inhibit mechanisms of synaptic plasticity that are believed to underlie learning and memory.

Blockade of << NMDA receptors >> by [[ memantine ]] could theoretically confer disease-modifying activity in AD by inhibiting the "weak" NMDA receptor-dependent excitotoxicity that has been hypothesized to play a role in the progressive neuronal loss that underlies the evolving dementia.

Blockade of NMDA receptors by << memantine >> could theoretically confer disease-modifying activity in AD by inhibiting the "weak" [[ NMDA receptor ]]-dependent excitotoxicity that has been hypothesized to play a role in the progressive neuronal loss that underlies the evolving dementia.

Moreover, recent in vitro studies suggest that << memantine >> abrogates [[ beta-amyloid ]] (Abeta) toxicity and possibly inhibits Abeta production.

Moreover, recent in vitro studies suggest that << memantine >> abrogates beta-amyloid ([[ Abeta ]]) toxicity and possibly inhibits Abeta production.