Imatinib (STI571, << Gleevec >>, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, [[ ABL ]], BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


Imatinib (STI571, << Gleevec >>, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, [[ BCR ]]-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


Imatinib (STI571, << Gleevec >>, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-[[ ABL ]], PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


Imatinib (STI571, << Gleevec >>, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, [[ PDGFRA ]], and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


Imatinib (STI571, << Gleevec >>, Glivec; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, PDGFRA, and [[ PDGFRB, ]] represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


Imatinib (STI571, Gleevec, << Glivec >>; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of [[ KIT ]], ABL, BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


Imatinib (STI571, Gleevec, << Glivec >>; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, [[ ABL ]], BCR-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


Imatinib (STI571, Gleevec, << Glivec >>; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, [[ BCR ]]-ABL, PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


Imatinib (STI571, Gleevec, << Glivec >>; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-[[ ABL ]], PDGFRA, and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


Imatinib (STI571, Gleevec, << Glivec >>; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, [[ PDGFRA ]], and PDGFRB, represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


Imatinib (STI571, Gleevec, << Glivec >>; Novartis Pharmaceuticals, East Hanover, NJ), a selective inhibitor of KIT, ABL, BCR-ABL, PDGFRA, and [[ PDGFRB, ]] represents a new paradigm of targeted cancer therapy and has revolutionized the treatment of patients with chronic myelogenous leukemia and GISTs.


Evaluation of histamine H1-, H2-, and H3-receptor ligands at the human histamine H4 receptor: identification of << 4-methylhistamine >> as the first potent and selective [[ H4 receptor ]] agonist.


Most of the tested H(2)R agonists and << imidazole >>-based H(3)R ligands show micromolar-to-nanomolar range hH(4)R affinity, and these ligands exert different intrinsic [[ hH(4)R ]] activities, ranging from full agonists to inverse agonists.


Moreover, << 4-methylhistamine >> potently activated the [[ hH(4)R ]] (pEC(50) = 7.4 +/- 0.1; alpha = 1), and this response was competitively antagonized by the selective H(4)R antagonist JNJ 7777120 [1-[(5-chloro-1H-indol-2-yl)-carbonyl]-4-methylpiperazine] (pA(2) = 7.8).


Moreover, 4-methylhistamine potently activated the hH(4)R (pEC(50) = 7.4 +/- 0.1; alpha = 1), and this response was competitively antagonized by the selective << H(4)R >> antagonist [[ JNJ 7777120 ]] [1-[(5-chloro-1H-indol-2-yl)-carbonyl]-4-methylpiperazine] (pA(2) = 7.8).


Moreover, 4-methylhistamine potently activated the hH(4)R (pEC(50) = 7.4 +/- 0.1; alpha = 1), and this response was competitively antagonized by the selective << H(4)R >> antagonist JNJ 7777120 [[[ 1-[(5-chloro-1H-indol-2-yl)-carbonyl]-4-methylpiperazine ]]] (pA(2) = 7.8).


The identification of << 4-methylhistamine >> as a potent [[ H(4)R ]] agonist is of major importance for future studies to unravel the physiological roles of the H(4)R.


Irinotecan (CPT-11, << 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin >>) has exhibited clinical activities against a broad spectrum of carcinomas by inhibiting [[ DNA topoisomerase I ]] (Topo I).


Irinotecan (CPT-11, << 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin >>) has exhibited clinical activities against a broad spectrum of carcinomas by inhibiting DNA topoisomerase I ([[ Topo I ]]).


<< Irinotecan >> (CPT-11, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin) has exhibited clinical activities against a broad spectrum of carcinomas by inhibiting [[ DNA topoisomerase I ]] (Topo I).


<< Irinotecan >> (CPT-11, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin) has exhibited clinical activities against a broad spectrum of carcinomas by inhibiting DNA topoisomerase I ([[ Topo I ]]).


Irinotecan (<< CPT-11 >>, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin) has exhibited clinical activities against a broad spectrum of carcinomas by inhibiting [[ DNA topoisomerase I ]] (Topo I).


Irinotecan (<< CPT-11 >>, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carbonyloxycamptothecin) has exhibited clinical activities against a broad spectrum of carcinomas by inhibiting DNA topoisomerase I ([[ Topo I ]]).


Early-onset diarrhea is observed immediately after CPT-11 infusion and probably due to the inhibition of << acetylcholinesterase >> activity, which can be eliminated by administration of [[ atropine ]].


Early-onset diarrhea is observed immediately after << CPT-11 >> infusion and probably due to the inhibition of [[ acetylcholinesterase ]] activity, which can be eliminated by administration of atropine.


<< CPT-11 >> and SN-38 may also stimulate the production of pro-inflammatory [[ cytokines ]] and prostaglandins (PGs), thus inducing the secretion of Na(+) and Cl(-).


CPT-11 and << SN-38 >> may also stimulate the production of pro-inflammatory [[ cytokines ]] and prostaglandins (PGs), thus inducing the secretion of Na(+) and Cl(-).


<< Pyridoxal kinase >> (PDXK) catalyzes the phosphorylation of [[ pyridoxal ]], pyridoxamine, and pyridoxine in the presence of ATP and Zn2+.


Pyridoxal kinase (<< PDXK >>) catalyzes the phosphorylation of [[ pyridoxal ]], pyridoxamine, and pyridoxine in the presence of ATP and Zn2+.


<< Pyridoxal kinase >> (PDXK) catalyzes the phosphorylation of pyridoxal, [[ pyridoxamine ]], and pyridoxine in the presence of ATP and Zn2+.


Pyridoxal kinase (<< PDXK >>) catalyzes the phosphorylation of pyridoxal, [[ pyridoxamine ]], and pyridoxine in the presence of ATP and Zn2+.


<< Pyridoxal kinase >> (PDXK) catalyzes the phosphorylation of pyridoxal, pyridoxamine, and [[ pyridoxine ]] in the presence of ATP and Zn2+.


Pyridoxal kinase (<< PDXK >>) catalyzes the phosphorylation of pyridoxal, pyridoxamine, and [[ pyridoxine ]] in the presence of ATP and Zn2+.


<< (R)-Roscovitine >> (CYC202, Seliciclib) is a relatively selective inhibitor of [[ cyclin-dependent kinases ]] (CDKs), currently evaluated for the treatment of cancers, neurodegenerative disorders, renal diseases, and several viral infections.


<< (R)-Roscovitine >> (CYC202, Seliciclib) is a relatively selective inhibitor of cyclin-dependent kinases ([[ CDKs ]]), currently evaluated for the treatment of cancers, neurodegenerative disorders, renal diseases, and several viral infections.


(R)-Roscovitine (<< CYC202 >>, Seliciclib) is a relatively selective inhibitor of [[ cyclin-dependent kinases ]] (CDKs), currently evaluated for the treatment of cancers, neurodegenerative disorders, renal diseases, and several viral infections.


(R)-Roscovitine (<< CYC202 >>, Seliciclib) is a relatively selective inhibitor of cyclin-dependent kinases ([[ CDKs ]]), currently evaluated for the treatment of cancers, neurodegenerative disorders, renal diseases, and several viral infections.


(R)-Roscovitine (CYC202, << Seliciclib >>) is a relatively selective inhibitor of [[ cyclin-dependent kinases ]] (CDKs), currently evaluated for the treatment of cancers, neurodegenerative disorders, renal diseases, and several viral infections.


(R)-Roscovitine (CYC202, << Seliciclib >>) is a relatively selective inhibitor of cyclin-dependent kinases ([[ CDKs ]]), currently evaluated for the treatment of cancers, neurodegenerative disorders, renal diseases, and several viral infections.


Using [(3)H]glucosamine-labeled gastric mucosal cells, we show that stimulatory effect of beta-adrenergic agonist, isoproterenol, on << mucin >> secretion was inhibited by EGFR kinase inhibitor, [[ PD153035 ]], as well as wortmannin, a specific inhibitor of PI3K.


Using [(3)H]glucosamine-labeled gastric mucosal cells, we show that stimulatory effect of beta-adrenergic agonist, isoproterenol, on << mucin >> secretion was inhibited by EGFR kinase inhibitor, PD153035, as well as [[ wortmannin ]], a specific inhibitor of PI3K.


Using [(3)H]glucosamine-labeled gastric mucosal cells, we show that stimulatory effect of beta-adrenergic agonist, isoproterenol, on mucin secretion was inhibited by << EGFR >> kinase inhibitor, [[ PD153035 ]], as well as wortmannin, a specific inhibitor of PI3K.


Using [(3)H]glucosamine-labeled gastric mucosal cells, we show that stimulatory effect of beta-adrenergic agonist, isoproterenol, on mucin secretion was inhibited by EGFR << kinase >> inhibitor, [[ PD153035 ]], as well as wortmannin, a specific inhibitor of PI3K.


Using [(3)H]glucosamine-labeled gastric mucosal cells, we show that stimulatory effect of beta-adrenergic agonist, isoproterenol, on mucin secretion was inhibited by EGFR kinase inhibitor, PD153035, as well as << wortmannin >>, a specific inhibitor of [[ PI3K ]].


Both inhibitors, moreover, blunted the mucin secretory responses to beta-adrenergic agonist-generated second messenger, cAMP as well as << adenylate cyclase >> activator, [[ forskolin ]].


Both inhibitors, moreover, blunted the << mucin >> secretory responses to beta-adrenergic agonist-generated second messenger, cAMP as well as adenylate cyclase activator, [[ forskolin ]].


Both inhibitors, moreover, blunted the mucin secretory responses to beta-adrenergic agonist-generated second messenger, << cAMP >> as well as [[ adenylate cyclase ]] activator, forskolin.


The gastric mucin secretory responses to isoproterenol, furthermore, were inhibited by << PP2 >>, a selective inhibitor of tyrosine kinase Src responsible for ligand-independent [[ EGFR ]] autophosphorylation, but not by ERK inhibitor, PD98059.


The << gastric mucin >> secretory responses to isoproterenol, furthermore, were inhibited by [[ PP2 ]], a selective inhibitor of tyrosine kinase Src responsible for ligand-independent EGFR autophosphorylation, but not by ERK inhibitor, PD98059.


The gastric mucin secretory responses to isoproterenol, furthermore, were inhibited by << PP2 >>, a selective inhibitor of [[ tyrosine kinase ]] Src responsible for ligand-independent EGFR autophosphorylation, but not by ERK inhibitor, PD98059.


The gastric mucin secretory responses to isoproterenol, furthermore, were inhibited by << PP2 >>, a selective inhibitor of tyrosine kinase [[ Src ]] responsible for ligand-independent EGFR autophosphorylation, but not by ERK inhibitor, PD98059.


The gastric mucin secretory responses to isoproterenol, furthermore, were inhibited by PP2, a selective inhibitor of tyrosine kinase Src responsible for ligand-independent EGFR autophosphorylation, but not by << ERK >> inhibitor, [[ PD98059 ]].


The inhibition of << ERK >>, moreover, did not cause attenuation in mucin secretion in response to [[ cAMP ]] and forskolin.


The inhibition of << ERK >>, moreover, did not cause attenuation in mucin secretion in response to cAMP and [[ forskolin ]].


<< Losartan >>: a selective [[ angiotensin II type 1 (AT1) receptor ]] antagonist for the treatment of heart failure.


<< Losartan >> (COZAAR) is the prototype of a new class of potent and selective [[ angiotensin II (AII) type 1 (AT(1)) receptor ]] antagonists with the largest published preclinical and clinical data base.


Losartan (<< COZAAR >>) is the prototype of a new class of potent and selective [[ angiotensin II (AII) type 1 (AT(1)) receptor ]] antagonists with the largest published preclinical and clinical data base.


<< Losartan >> is well-absorbed orally as an active drug and is rapidly converted via oxidation in the human liver to a more potent metabolite (designated E3174) with an affinity 20- to 30-times greater for the [[ AT(1) receptor ]] (non-competitive inhibition).


Clinical experience in heart failure is growing, and recent data suggest an improved survival with << losartan >> versus captopril, a drug from the [[ angiotensin-converting-enzyme ]] inhibitor class with proven benefit in this population.


Clinical experience in heart failure is growing, and recent data suggest an improved survival with losartan versus << captopril >>, a drug from the [[ angiotensin-converting-enzyme ]] inhibitor class with proven benefit in this population.


The current comprehensive losartan clinical end-point programme (4 large scale morbidity/mortality trials) should provide evidence regarding the efficacy of direct blockade of the << AT(1) receptor >> with [[ losartan ]] compared to standard therapy: 1) The Losartan Heart Failure Survival Study - ELITE II, 2) The Losartan Post-Myocardial Infarction Survival Study - OPTIMAAL, 3) The Losartan Hypertension Survival Study - LIFE and 4) The Losartan Renal Protection Study - RENAAL.


We now demonstrate that << amrinone >>, a noncatechol inotrope, strongly inhibits lipopolysaccharide (LPS)-induced [[ TNF ]] production at concentrations readily achieved in vivo.


Combined application of << dexamethasone >> and amrinone caused additive inhibition of [[ TNF ]] biosynthesis in vitro.


Combined application of dexamethasone and << amrinone >> caused additive inhibition of [[ TNF ]] biosynthesis in vitro.


Abrupt removal of << amrinone >> or pentoxifylline from the culture medium prior to LPS stimulation, however, caused significantly augmented [[ TNF ]] production.


Abrupt removal of amrinone or << pentoxifylline >> from the culture medium prior to LPS stimulation, however, caused significantly augmented [[ TNF ]] production.


In the present study, age-related changes of << pyridoxal 5'-phosphate >> (PLP) synthesizing enzymes, pyridoxal kinase ([[ PLK ]]) and pyridoxine 5'-phosphate oxidase (PNPO), their protein contents and activities were examined in the gerbil hippocampus proper.


In the present study, age-related changes of << pyridoxal 5'-phosphate >> (PLP) synthesizing enzymes, pyridoxal kinase (PLK) and [[ pyridoxine 5'-phosphate oxidase ]] (PNPO), their protein contents and activities were examined in the gerbil hippocampus proper.


In the present study, age-related changes of << pyridoxal 5'-phosphate >> (PLP) synthesizing enzymes, pyridoxal kinase (PLK) and pyridoxine 5'-phosphate oxidase ([[ PNPO ]]), their protein contents and activities were examined in the gerbil hippocampus proper.


In the present study, age-related changes of << pyridoxal 5'-phosphate >> (PLP) synthesizing enzymes, [[ pyridoxal kinase ]] (PLK) and pyridoxine 5'-phosphate oxidase (PNPO), their protein contents and activities were examined in the gerbil hippocampus proper.


In the present study, age-related changes of pyridoxal 5'-phosphate (<< PLP >>) synthesizing enzymes, pyridoxal kinase ([[ PLK ]]) and pyridoxine 5'-phosphate oxidase (PNPO), their protein contents and activities were examined in the gerbil hippocampus proper.


In the present study, age-related changes of pyridoxal 5'-phosphate (<< PLP >>) synthesizing enzymes, pyridoxal kinase (PLK) and [[ pyridoxine 5'-phosphate oxidase ]] (PNPO), their protein contents and activities were examined in the gerbil hippocampus proper.


In the present study, age-related changes of pyridoxal 5'-phosphate (<< PLP >>) synthesizing enzymes, pyridoxal kinase (PLK) and pyridoxine 5'-phosphate oxidase ([[ PNPO ]]), their protein contents and activities were examined in the gerbil hippocampus proper.


In the present study, age-related changes of pyridoxal 5'-phosphate (<< PLP >>) synthesizing enzymes, [[ pyridoxal kinase ]] (PLK) and pyridoxine 5'-phosphate oxidase (PNPO), their protein contents and activities were examined in the gerbil hippocampus proper.


Therefore, decreases of << PLK >> and PNPO in the hippocampal CA1 region of aged brains may be involved in aging processes related with [[ gamma-aminobutyric acid ]] (GABA) function.


Therefore, decreases of PLK and << PNPO >> in the hippocampal CA1 region of aged brains may be involved in aging processes related with [[ gamma-aminobutyric acid ]] (GABA) function.


Therefore, decreases of << PLK >> and PNPO in the hippocampal CA1 region of aged brains may be involved in aging processes related with gamma-aminobutyric acid ([[ GABA ]]) function.


Therefore, decreases of PLK and << PNPO >> in the hippocampal CA1 region of aged brains may be involved in aging processes related with gamma-aminobutyric acid ([[ GABA ]]) function.


This process was reduced by a protonophore, carbonylcyanide p-trifluoromethoxyphenylhydrazone, and a typical << monocarboxylate transporter >> (MCT) inhibitor, [[ alpha-cyano-4-hydroxycinnamic acid ]], suggesting that nicotinate uptake by rat astrocytes is mediated by H(+)-coupled monocarboxylate transport system.


This process was reduced by a protonophore, carbonylcyanide p-trifluoromethoxyphenylhydrazone, and a typical monocarboxylate transporter (<< MCT >>) inhibitor, [[ alpha-cyano-4-hydroxycinnamic acid ]], suggesting that nicotinate uptake by rat astrocytes is mediated by H(+)-coupled monocarboxylate transport system.


This process was reduced by a protonophore, carbonylcyanide p-trifluoromethoxyphenylhydrazone, and a typical monocarboxylate transporter (MCT) inhibitor, alpha-cyano-4-hydroxycinnamic acid, suggesting that << nicotinate >> uptake by rat astrocytes is mediated by H(+)-coupled [[ monocarboxylate transport system ]].


Because l-lactate reduced to 67% of the nicotinate uptake even at 10mM, it is unlikely that << nicotinate >> uptake in rat astrocytes is mediated by [[ MCT1 ]] and/or MCT2.


Because l-lactate reduced to 67% of the nicotinate uptake even at 10mM, it is unlikely that << nicotinate >> uptake in rat astrocytes is mediated by MCT1 and/or [[ MCT2 ]].


These results provide biochemical evidence of a H(+)-coupled and saturable transport system, presumed to be a << low-affinity monocarboxylate transporter >> MCT4 or other unknown H(+)-coupled monocarboxylate transport system, for [[ nicotinate ]] in rat cerebrocortical astrocytes.


These results provide biochemical evidence of a H(+)-coupled and saturable transport system, presumed to be a low-affinity monocarboxylate transporter << MCT4 >> or other unknown H(+)-coupled monocarboxylate transport system, for [[ nicotinate ]] in rat cerebrocortical astrocytes.


These results provide biochemical evidence of a H(+)-coupled and saturable transport system, presumed to be a low-affinity monocarboxylate transporter MCT4 or other unknown << H(+)-coupled monocarboxylate transport system >>, for [[ nicotinate ]] in rat cerebrocortical astrocytes.


A review of the structural and functional features of << olmesartan medoxomil >>, an [[ angiotensin receptor ]] blocker.


The marked antihypertensive efficacy of << olmesartan medoxomil >> may result from a unique pharmacological interaction of the drug with the AT1 receptor, resulting in a potent, long-lasting, dose-dependent blockade of [[ A-II ]].


Effects of << granulocyte colony-stimulating factor >> (G-CSF) and neutrophil elastase inhibitor ([[ ONO-5046 ]]) on acid-induced lung injury in rats.


Effects of granulocyte colony-stimulating factor (<< G-CSF >>) and neutrophil elastase inhibitor ([[ ONO-5046 ]]) on acid-induced lung injury in rats.


Effects of granulocyte colony-stimulating factor (G-CSF) and << neutrophil elastase >> inhibitor ([[ ONO-5046 ]]) on acid-induced lung injury in rats.


We examined the effects of the high dose of granulocyte-colony stimulating factor (G-CSF), which is capable of increasing peripheral neutrophils, and a specific << neutrophil elastase >> inhibitor ([[ ONO-5046 ]]) on acid lung injury in rats.


<< Miglustat >>, an imino sugar that reversibly inhibits [[ glucosylceramide synthase ]] and reduces intracellular substrate burden, is an oral treatment for patients with type 1 GD that was recently approved in the United States for symptomatic patients with mild to moderate clinical manifestations for whom ERT is not an option.


Miglustat, an << imino sugar >> that reversibly inhibits [[ glucosylceramide synthase ]] and reduces intracellular substrate burden, is an oral treatment for patients with type 1 GD that was recently approved in the United States for symptomatic patients with mild to moderate clinical manifestations for whom ERT is not an option.


Nicotinic-receptor potentiator drugs, huprine X and << galantamine >>, increase ACh release by blocking [[ AChE ]] activity but not acting on nicotinic receptors.


This effect was reverted in the presence of << atropine >> (ATR; 0.1 microM), which blocks the pre-synaptic [[ muscarinic M2 receptor ]].


This effect was reverted in the presence of atropine (<< ATR >>; 0.1 microM), which blocks the pre-synaptic [[ muscarinic M2 receptor ]].


After that, a wide range of concentrations of drugs, concomitantly with ATR (0.1 microM), was studied in the presence of << haloperidol >> (HAL; 0.01 microM), a [[ dopamine D2 ]] antagonist.


After that, a wide range of concentrations of drugs, concomitantly with ATR (0.1 microM), was studied in the presence of haloperidol (<< HAL >>; 0.01 microM), a [[ dopamine D2 ]] antagonist.


To test the role of << nicotinic receptors >> in the drugs' effects on [3H]-ACh release, [[ mecamylamine ]] (MEC) 100 microM was used to block such receptors.


To test the role of << nicotinic receptors >> in the drugs' effects on [3H]-ACh release, mecamylamine ([[ MEC ]]) 100 microM was used to block such receptors.


mRNA levels for << RAR-alpha >>, RAR-beta and RAR-gamma, the nuclear receptors for retinoic acid, decreased during activation of freshly isolated HSC even with [[ retinoid ]] supplementation.


mRNA levels for RAR-alpha, << RAR-beta >> and RAR-gamma, the nuclear receptors for retinoic acid, decreased during activation of freshly isolated HSC even with [[ retinoid ]] supplementation.


mRNA levels for RAR-alpha, RAR-beta and << RAR-gamma >>, the nuclear receptors for retinoic acid, decreased during activation of freshly isolated HSC even with [[ retinoid ]] supplementation.


mRNA levels for RAR-alpha, RAR-beta and RAR-gamma, the << nuclear receptors >> for retinoic acid, decreased during activation of freshly isolated HSC even with [[ retinoid ]] supplementation.


Preincubation (30 min) of bovine tracheal smooth muscle with various concentrations (0.1, 1 and 10 microM) of << fenoterol >> decreased isoprenaline-induced maximal relaxation (E(max)) of methacholine-contracted preparations in a concentration dependent fashion, indicating desensitization of the [[ beta(2)-adrenoceptor ]].


Preincubation (30 min) of bovine tracheal smooth muscle with various concentrations (0.1, 1 and 10 microM) of fenoterol decreased << isoprenaline >>-induced maximal relaxation (E(max)) of methacholine-contracted preparations in a concentration dependent fashion, indicating desensitization of the [[ beta(2)-adrenoceptor ]].


Preincubation with 1 microM of the << protein kinase C >> (PKC) activator phorbol 12-myristate 13-acetate ([[ PMA ]]) caused a small but significant decrease in isoprenaline-induced E(max), indicating activated PKC-mediated heterologous beta(2)-adrenoceptor desensitization.


Preincubation with 1 microM of the protein kinase C (<< PKC >>) activator phorbol 12-myristate 13-acetate ([[ PMA ]]) caused a small but significant decrease in isoprenaline-induced E(max), indicating activated PKC-mediated heterologous beta(2)-adrenoceptor desensitization.


Preincubation with 1 microM of the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (<< PMA >>) caused a small but significant decrease in isoprenaline-induced E(max), indicating activated [[ PKC ]]-mediated heterologous beta(2)-adrenoceptor desensitization.


Preincubation with 1 microM of the << protein kinase C >> (PKC) activator [[ phorbol 12-myristate 13-acetate ]] (PMA) caused a small but significant decrease in isoprenaline-induced E(max), indicating activated PKC-mediated heterologous beta(2)-adrenoceptor desensitization.


Preincubation with 1 microM of the protein kinase C (<< PKC >>) activator [[ phorbol 12-myristate 13-acetate ]] (PMA) caused a small but significant decrease in isoprenaline-induced E(max), indicating activated PKC-mediated heterologous beta(2)-adrenoceptor desensitization.


Preincubation with 1 microM of the protein kinase C (PKC) activator << phorbol 12-myristate 13-acetate >> (PMA) caused a small but significant decrease in isoprenaline-induced E(max), indicating activated [[ PKC ]]-mediated heterologous beta(2)-adrenoceptor desensitization.


Preincubation with 1 microM of the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (<< PMA >>) caused a small but significant decrease in isoprenaline-induced E(max), indicating activated PKC-mediated heterologous [[ beta(2)-adrenoceptor ]] desensitization.


Preincubation with 1 microM of the protein kinase C (PKC) activator << phorbol 12-myristate 13-acetate >> (PMA) caused a small but significant decrease in isoprenaline-induced E(max), indicating activated PKC-mediated heterologous [[ beta(2)-adrenoceptor ]] desensitization.


Preincubation with 1 microM of the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) caused a small but significant decrease in << isoprenaline >>-induced E(max), indicating activated PKC-mediated heterologous [[ beta(2)-adrenoceptor ]] desensitization.


Moreover, the specific << PKC >>-inhibitor [[ 2-[1-(3-dimethylaminopropyl)-1H-indol-3-yl]-3-(1H-indol-3-yl) maleimide ]] (GF 109203X) markedly increased the potency and E(max) of isoprenaline for all conditions used, including control conditions, and the synergistic effects of PMA and fenoterol were completely prevented.


Moreover, the specific << PKC >>-inhibitor 2-[1-(3-dimethylaminopropyl)-1H-indol-3-yl]-3-(1H-indol-3-yl) maleimide ([[ GF 109203X ]]) markedly increased the potency and E(max) of isoprenaline for all conditions used, including control conditions, and the synergistic effects of PMA and fenoterol were completely prevented.


Tyrosine kinase inhibitors are << quinazoline >>-derived, low molecular weight synthetic molecules that can block the intracellular tyrosine kinase domain of several receptors, including EGFR, Erb2, and vascular endothelial growth factor receptor, and thereby inhibit ligand-induced receptor phosphorylation and abrogate the biologic effect of [[ EGFR ]] signaling.


<< Tyrosine kinase >> inhibitors are [[ quinazoline ]]-derived, low molecular weight synthetic molecules that can block the intracellular tyrosine kinase domain of several receptors, including EGFR, Erb2, and vascular endothelial growth factor receptor, and thereby inhibit ligand-induced receptor phosphorylation and abrogate the biologic effect of EGFR signaling.


Tyrosine kinase inhibitors are << quinazoline >>-derived, low molecular weight synthetic molecules that can block the intracellular [[ tyrosine kinase domain ]] of several receptors, including EGFR, Erb2, and vascular endothelial growth factor receptor, and thereby inhibit ligand-induced receptor phosphorylation and abrogate the biologic effect of EGFR signaling.


Tyrosine kinase inhibitors are << quinazoline >>-derived, low molecular weight synthetic molecules that can block the intracellular tyrosine kinase domain of several receptors, including [[ EGFR ]], Erb2, and vascular endothelial growth factor receptor, and thereby inhibit ligand-induced receptor phosphorylation and abrogate the biologic effect of EGFR signaling.


Tyrosine kinase inhibitors are << quinazoline >>-derived, low molecular weight synthetic molecules that can block the intracellular tyrosine kinase domain of several receptors, including EGFR, [[ Erb2 ]], and vascular endothelial growth factor receptor, and thereby inhibit ligand-induced receptor phosphorylation and abrogate the biologic effect of EGFR signaling.


Tyrosine kinase inhibitors are << quinazoline >>-derived, low molecular weight synthetic molecules that can block the intracellular tyrosine kinase domain of several receptors, including EGFR, Erb2, and [[ vascular endothelial growth factor receptor ]], and thereby inhibit ligand-induced receptor phosphorylation and abrogate the biologic effect of EGFR signaling.


When expressed heterologously in a mammalian cell line, << rabbit PAT1 >> mediates pH-dependent, Na(+)-independent uptake of [[ proline ]], glycine, l-alanine and alpha-(methylamino)isobutyric acid.


When expressed heterologously in a mammalian cell line, << rabbit PAT1 >> mediates pH-dependent, Na(+)-independent uptake of proline, [[ glycine ]], l-alanine and alpha-(methylamino)isobutyric acid.


When expressed heterologously in a mammalian cell line, << rabbit PAT1 >> mediates pH-dependent, Na(+)-independent uptake of proline, glycine, [[ l-alanine ]] and alpha-(methylamino)isobutyric acid.


When expressed heterologously in a mammalian cell line, << rabbit PAT1 >> mediates pH-dependent, Na(+)-independent uptake of proline, glycine, l-alanine and [[ alpha-(methylamino)isobutyric acid ]].


In the presence of Na+ and under conditions in which << PAT1 >> transport function was suppressed, a second [[ proline ]] uptake system was detected that exhibited functional characteristics similar to those of the IMINO system.


The functional characteristics of rabbit PAT1 in either mammalian cells or renal BBMV suggest that << PAT1 >> is the low-affinity transporter of [[ proline ]], glycine and hydroxyproline believed to be defective in patients with iminoglycinuria.


The functional characteristics of rabbit PAT1 in either mammalian cells or renal BBMV suggest that << PAT1 >> is the low-affinity transporter of proline, [[ glycine ]] and hydroxyproline believed to be defective in patients with iminoglycinuria.


The functional characteristics of rabbit PAT1 in either mammalian cells or renal BBMV suggest that << PAT1 >> is the low-affinity transporter of proline, glycine and [[ hydroxyproline ]] believed to be defective in patients with iminoglycinuria.


The fact that << trimipramine >> also suppressed [[ IFN-gamma ]] production and T-cell proliferation indicates that these immunomodulatory actions of antidepressants are most likely unrelated to inhibition of monoamine reuptake.


The mean body weight at baseline (52.59 kg) did not differ significantly from that at 1 week after treatment (52.84 kg; P > .05), but the mean << leptin >> level after 1 week of treatment with [[ cyproheptadine ]] (3.14 ng/mL) was 14.2% higher than that at baseline (2.75 ng/mL; P < .05).


Comparison of << captopril >> and enalapril to study the role of the sulfhydryl-group in improvement of endothelial dysfunction with [[ ACE ]] inhibitors in high dieted methionine mice.


Comparison of captopril and << enalapril >> to study the role of the sulfhydryl-group in improvement of endothelial dysfunction with [[ ACE ]] inhibitors in high dieted methionine mice.


Comparison of captopril and enalapril to study the role of the << sulfhydryl >>-group in improvement of endothelial dysfunction with [[ ACE ]] inhibitors in high dieted methionine mice.


We compared the effects of << Captopril >> (an [[ ACE ]] inhibitor with -SH group), enalapril (an ACE-inhibitor without -SH group), N-acetylcysteine (only -SH group not ACE inhibitor) on endothelial dysfunction injured by methionine-induced hyperhomocysteinemia (HHcy) in rats.


We compared the effects of Captopril (an << ACE >> inhibitor with -[[ SH ]] group), enalapril (an ACE-inhibitor without -SH group), N-acetylcysteine (only -SH group not ACE inhibitor) on endothelial dysfunction injured by methionine-induced hyperhomocysteinemia (HHcy) in rats.


We compared the effects of Captopril (an ACE inhibitor with -SH group), << enalapril >> (an [[ ACE ]]-inhibitor without -SH group), N-acetylcysteine (only -SH group not ACE inhibitor) on endothelial dysfunction injured by methionine-induced hyperhomocysteinemia (HHcy) in rats.


It was found that a single intragastric gavage by << L-methionine >> resulted in inhibition of endothelium-dependent relaxation, markedly increased the serum level of malondialdehyde and decreased the activity of [[ PON1 ]] and SOD, similarly decreased the level of NO in the serum; but had no effects on endothelium-independent relaxation and angiotensin-converting enzyme activity compared with the control group.


It was found that a single intragastric gavage by << L-methionine >> resulted in inhibition of endothelium-dependent relaxation, markedly increased the serum level of malondialdehyde and decreased the activity of PON1 and [[ SOD ]], similarly decreased the level of NO in the serum; but had no effects on endothelium-independent relaxation and angiotensin-converting enzyme activity compared with the control group.


Given the treatment with three doses of << Captopril >> (15 approximately 45 mg/kg) markedly attenuated inhibition of vasodilator responses to ACh, and eliminated the increased level of malondialdehyde, the decreased level of NO, activity of [[ PON1 ]] and SOD in serum by single intragastric gavaged L-methionine.


Given the treatment with three doses of << Captopril >> (15 approximately 45 mg/kg) markedly attenuated inhibition of vasodilator responses to ACh, and eliminated the increased level of malondialdehyde, the decreased level of NO, activity of PON1 and [[ SOD ]] in serum by single intragastric gavaged L-methionine.


These results suggested that Captopril can protect the vascular endothelium against the damages induced by L-methionine in rats, and the beneficial effects of << Captopril >> may be related to attenuating the decrease in [[ PON1 ]] activity and NO levels.


These results suggested that Captopril can protect the vascular endothelium against the damages induced by << L-methionine >> in rats, and the beneficial effects of Captopril may be related to attenuating the decrease in [[ PON1 ]] activity and NO levels.


<< Sorafenib >>, which belongs chemically to a class that can be described as bis-aryl ureas, was selected for further pharmacologic characterization based on potent inhibition of [[ Raf-1 ]] and its favorable kinase selectivity profile.


<< Sorafenib >>, which belongs chemically to a class that can be described as bis-aryl ureas, was selected for further pharmacologic characterization based on potent inhibition of Raf-1 and its favorable [[ kinase ]] selectivity profile.


Sorafenib, which belongs chemically to a class that can be described as << bis-aryl ureas >>, was selected for further pharmacologic characterization based on potent inhibition of [[ Raf-1 ]] and its favorable kinase selectivity profile.


Sorafenib, which belongs chemically to a class that can be described as << bis-aryl ureas >>, was selected for further pharmacologic characterization based on potent inhibition of Raf-1 and its favorable [[ kinase ]] selectivity profile.


Further characterization showed that << sorafenib >> suppresses both wild-type and [[ V599E ]] mutant B-Raf activity in vitro.


Further characterization showed that << sorafenib >> suppresses both wild-type and V599E mutant [[ B-Raf ]] activity in vitro.


In addition, << sorafenib >> demonstrated significant activity against several receptor tyrosine kinases involved in neovascularization and tumor progression, including vascular-endothelial growth factor (VEGFR)-2, [[ VEGFR-3 ]], platelet-derived growth factor (PDGFR)-beta Flt-3, and c-KIT.


In addition, << sorafenib >> demonstrated significant activity against several receptor tyrosine kinases involved in neovascularization and tumor progression, including vascular-endothelial growth factor (VEGFR)-2, VEGFR-3, [[ platelet-derived growth factor (PDGFR)-beta ]] Flt-3, and c-KIT.


In addition, << sorafenib >> demonstrated significant activity against several receptor tyrosine kinases involved in neovascularization and tumor progression, including vascular-endothelial growth factor (VEGFR)-2, VEGFR-3, platelet-derived growth factor (PDGFR)-beta [[ Flt-3 ]], and c-KIT.


In addition, << sorafenib >> demonstrated significant activity against several receptor tyrosine kinases involved in neovascularization and tumor progression, including vascular-endothelial growth factor (VEGFR)-2, VEGFR-3, platelet-derived growth factor (PDGFR)-beta Flt-3, and [[ c-KIT ]].


In addition, << sorafenib >> demonstrated significant activity against several [[ receptor tyrosine kinases ]] involved in neovascularization and tumor progression, including vascular-endothelial growth factor (VEGFR)-2, VEGFR-3, platelet-derived growth factor (PDGFR)-beta Flt-3, and c-KIT.


In addition, << sorafenib >> demonstrated significant activity against several receptor tyrosine kinases involved in neovascularization and tumor progression, including [[ vascular-endothelial growth factor (VEGFR)-2 ]], VEGFR-3, platelet-derived growth factor (PDGFR)-beta Flt-3, and c-KIT.


A selective << retinoid X receptor >> agonist [[ bexarotene ]] (LGD1069, targretin) inhibits angiogenesis and metastasis in solid tumours.


A selective << retinoid X receptor >> agonist bexarotene ([[ LGD1069 ]], targretin) inhibits angiogenesis and metastasis in solid tumours.


A selective << retinoid X receptor >> agonist bexarotene (LGD1069, [[ targretin ]]) inhibits angiogenesis and metastasis in solid tumours.


The present study determined the influence of a << retinoid X receptor >> agonist [[ bexarotene ]] on angiogenesis and metastasis in solid tumours.


Analysis of tumour-conditioned medium indicated that << bexarotene >> decreased the secretion of angiogenic factors and matrix metalloproteinases and increased the tissue inhibitor of [[ matrix metalloproteinases ]].


Analysis of tumour-conditioned medium indicated that << bexarotene >> decreased the secretion of angiogenic factors and [[ matrix metalloproteinases ]] and increased the tissue inhibitor of matrix metalloproteinases.


The ability of << bexarotene >> to inhibit angiogenesis and metastasis was dependent on activation of its heterodimerisation partner [[ peroxisome proliferator-activated receptor gamma ]].


In subjects with dysmenorrhea the increase in pain following the administration of << vasopressin >> was significantly lower during [[ atosiban ]] than during placebo infusion.


CONCLUSIONS: << Atosiban >> reduces [[ vasopressin ]]-induced intrauterine pressure in both healthy volunteers and dysmenorrheics, and reported pain in subjects with dysmenorrhea.


Novel highly affine histamine H3 receptor ligands with additional inhibitory effects on the main histamine metabolizing enzyme in the brain, N-methyltransferase, chemically show structural elements of the << acetylcholinesterase >> inhibitor [[ tacrine ]].


Novel highly affine histamine H3 receptor ligands with additional inhibitory effects on the main << histamine >> metabolizing enzyme in the brain, [[ N-methyltransferase ]], chemically show structural elements of the acetylcholinesterase inhibitor tacrine.


Some of the new compounds proved in a slightly modified colorimetric Ellmann's assay to be potent inhibitors of << acetylcholinesterase >> and of butyrylcholinesterase which is another catalytic enzyme hydrolysing [[ acetylcholine ]].


Some of the new compounds proved in a slightly modified colorimetric Ellmann's assay to be potent inhibitors of acetylcholinesterase and of << butyrylcholinesterase >> which is another catalytic enzyme hydrolysing [[ acetylcholine ]].


For some, pharmacologic inhibitors are available, including << sorafenib >> for [[ BRAF ]], farnesyltransferase inhibitors for NRAS, PD-0325901 for mitogen-activated protein kinase/extracellular signal-regulated kinase kinase, rapamycin analogues for mammalian target of rapamycin, and agents that inhibit either vascular endothelial growth factor or its receptors.


For some, pharmacologic inhibitors are available, including sorafenib for BRAF, farnesyltransferase inhibitors for NRAS, << PD-0325901 >> for [[ mitogen-activated protein kinase ]]/extracellular signal-regulated kinase kinase, rapamycin analogues for mammalian target of rapamycin, and agents that inhibit either vascular endothelial growth factor or its receptors.


For some, pharmacologic inhibitors are available, including sorafenib for BRAF, farnesyltransferase inhibitors for NRAS, << PD-0325901 >> for mitogen-activated protein kinase/[[ extracellular signal-regulated kinase kinase ]], rapamycin analogues for mammalian target of rapamycin, and agents that inhibit either vascular endothelial growth factor or its receptors.


For some, pharmacologic inhibitors are available, including sorafenib for BRAF, farnesyltransferase inhibitors for NRAS, PD-0325901 for mitogen-activated protein kinase/extracellular signal-regulated kinase kinase, << rapamycin >> analogues for [[ mammalian target of rapamycin ]], and agents that inhibit either vascular endothelial growth factor or its receptors.


This aminophospholipid "<< flippase >>" selectively transports [[ PS ]] to the cytosolic leaflet of the bilayer and is sensitive to vanadate, Ca(2+), and modification by sulfhydryl reagents.


The purified << Atp8a1 >> is inactive in detergent micelles or in micelles containing phosphatidylcholine, phosphatidic acid, or phosphatidylinositol, is minimally activated by [[ phosphatidylglycerol ]] or phosphatidylethanolamine (PE), and is maximally activated by PS.


The purified << Atp8a1 >> is inactive in detergent micelles or in micelles containing phosphatidylcholine, phosphatidic acid, or phosphatidylinositol, is minimally activated by phosphatidylglycerol or [[ phosphatidylethanolamine ]] (PE), and is maximally activated by PS.


The purified << Atp8a1 >> is inactive in detergent micelles or in micelles containing phosphatidylcholine, phosphatidic acid, or phosphatidylinositol, is minimally activated by phosphatidylglycerol or phosphatidylethanolamine ([[ PE ]]), and is maximally activated by PS.


The purified << Atp8a1 >> is inactive in detergent micelles or in micelles containing phosphatidylcholine, phosphatidic acid, or phosphatidylinositol, is minimally activated by phosphatidylglycerol or phosphatidylethanolamine (PE), and is maximally activated by [[ PS ]].


Similar to the << plasma membrane PS transporter >>, Atp8a1 is activated only by the naturally occurring [[ sn-1,2-glycerol ]] isomer of PS and not the sn-2,3-glycerol stereoisomer.


Similar to the plasma membrane PS transporter, << Atp8a1 >> is activated only by the naturally occurring [[ sn-1,2-glycerol ]] isomer of PS and not the sn-2,3-glycerol stereoisomer.


Activation of << Atp8a1 >> is also reduced by these modifications; [[ phosphatidylserine-O-methyl ester ]], lysophosphatidylserine, glycerophosphoserine, and phosphoserine, which are not transported by the plasma membrane flippase, do not activate Atp8a1.


Activation of << Atp8a1 >> is also reduced by these modifications; phosphatidylserine-O-methyl ester, [[ lysophosphatidylserine ]], glycerophosphoserine, and phosphoserine, which are not transported by the plasma membrane flippase, do not activate Atp8a1.


Activation of << Atp8a1 >> is also reduced by these modifications; phosphatidylserine-O-methyl ester, lysophosphatidylserine, [[ glycerophosphoserine ]], and phosphoserine, which are not transported by the plasma membrane flippase, do not activate Atp8a1.


Activation of << Atp8a1 >> is also reduced by these modifications; phosphatidylserine-O-methyl ester, lysophosphatidylserine, glycerophosphoserine, and [[ phosphoserine ]], which are not transported by the plasma membrane flippase, do not activate Atp8a1.


Weakly translocated lipids (<< PE >>, phosphatidylhydroxypropionate, and phosphatidylhomoserine) are also weak [[ Atp8a1 ]] activators.


Weakly translocated lipids (PE, << phosphatidylhydroxypropionate >>, and phosphatidylhomoserine) are also weak [[ Atp8a1 ]] activators.


Weakly translocated lipids (PE, phosphatidylhydroxypropionate, and << phosphatidylhomoserine >>) are also weak [[ Atp8a1 ]] activators.


However, << N-methyl-phosphatidylserine >>, which is transported by the plasma membrane [[ flippase ]] at a rate equivalent to PS, is incapable of activating Atp8a1 activity.


These results indicate that the << ATPase >> activity of the secretory granule Atp8a1 is activated by phospholipids binding to a specific site whose properties ([[ PS ]] selectivity, dependence upon glycerol but not serine, stereochemistry, and vanadate sensitivity) are similar to, but distinct from, the properties of the substrate binding site of the plasma membrane flippase.


These results indicate that the ATPase activity of the secretory granule << Atp8a1 >> is activated by phospholipids binding to a specific site whose properties ([[ PS ]] selectivity, dependence upon glycerol but not serine, stereochemistry, and vanadate sensitivity) are similar to, but distinct from, the properties of the substrate binding site of the plasma membrane flippase.


<< Sorafenib >> (BAY 43-9006) is a small-molecule inhibitor that has been shown to target members of multiple classes of [[ tyrosine kinases ]] that are known to be involved in tumor cell proliferation and tumor angiogenesis.


Sorafenib (<< BAY 43-9006 >>) is a small-molecule inhibitor that has been shown to target members of multiple classes of [[ tyrosine kinases ]] that are known to be involved in tumor cell proliferation and tumor angiogenesis.


<< Hydrogen sulfide >> inhibits nitric oxide production and [[ nuclear factor-kappaB ]] via heme oxygenase-1 expression in RAW264.7 macrophages stimulated with lipopolysaccharide.


Hydrogen sulfide (<< H(2)S >>), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase ([[ CSE ]]) and/or cystathionine beta-synthase (CBS) from L-cysteine (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.


Hydrogen sulfide (<< H(2)S >>), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (CSE) and/or [[ cystathionine beta-synthase ]] (CBS) from L-cysteine (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.


Hydrogen sulfide (<< H(2)S >>), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (CSE) and/or cystathionine beta-synthase ([[ CBS ]]) from L-cysteine (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.


Hydrogen sulfide (<< H(2)S >>), a regulatory gaseous molecule that is endogenously synthesized by [[ cystathionine gamma-lyase ]] (CSE) and/or cystathionine beta-synthase (CBS) from L-cysteine (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.


<< Hydrogen sulfide >> (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase ([[ CSE ]]) and/or cystathionine beta-synthase (CBS) from L-cysteine (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.


<< Hydrogen sulfide >> (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (CSE) and/or [[ cystathionine beta-synthase ]] (CBS) from L-cysteine (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.


<< Hydrogen sulfide >> (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (CSE) and/or cystathionine beta-synthase ([[ CBS ]]) from L-cysteine (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.


<< Hydrogen sulfide >> (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by [[ cystathionine gamma-lyase ]] (CSE) and/or cystathionine beta-synthase (CBS) from L-cysteine (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.


Hydrogen sulfide (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (<< CSE >>) and/or cystathionine beta-synthase (CBS) from [[ L-cysteine ]] (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.


Hydrogen sulfide (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (CSE) and/or << cystathionine beta-synthase >> (CBS) from [[ L-cysteine ]] (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.


Hydrogen sulfide (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (CSE) and/or cystathionine beta-synthase (<< CBS >>) from [[ L-cysteine ]] (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.


Hydrogen sulfide (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by << cystathionine gamma-lyase >> (CSE) and/or cystathionine beta-synthase (CBS) from [[ L-cysteine ]] (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.


Hydrogen sulfide (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (<< CSE >>) and/or cystathionine beta-synthase (CBS) from L-cysteine ([[ L-Cys ]]) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.


Hydrogen sulfide (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (CSE) and/or << cystathionine beta-synthase >> (CBS) from L-cysteine ([[ L-Cys ]]) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.


Hydrogen sulfide (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (CSE) and/or cystathionine beta-synthase (<< CBS >>) from L-cysteine ([[ L-Cys ]]) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.


Hydrogen sulfide (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by << cystathionine gamma-lyase >> (CSE) and/or cystathionine beta-synthase (CBS) from L-cysteine ([[ L-Cys ]]) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored.


Here, we show that at noncytotoxic concentrations, << H(2)S >> was able to inhibit NO production and [[ inducible NO synthase ]] (iNOS) expression via heme oxygenase (HO-1) expression in RAW264.7 macrophages stimulated with lipopolysaccharide (LPS).


Here, we show that at noncytotoxic concentrations, << H(2)S >> was able to inhibit NO production and inducible NO synthase ([[ iNOS ]]) expression via heme oxygenase (HO-1) expression in RAW264.7 macrophages stimulated with lipopolysaccharide (LPS).


Here, we show that at noncytotoxic concentrations, H(2)S was able to inhibit << NO >> production and [[ inducible NO synthase ]] (iNOS) expression via heme oxygenase (HO-1) expression in RAW264.7 macrophages stimulated with lipopolysaccharide (LPS).


Here, we show that at noncytotoxic concentrations, H(2)S was able to inhibit << NO >> production and inducible NO synthase ([[ iNOS ]]) expression via heme oxygenase (HO-1) expression in RAW264.7 macrophages stimulated with lipopolysaccharide (LPS).


Both << H(2)S >> solution prepared by bubbling pure H(2)S gas and NaSH, a H(2)S donor, dose dependently induced HO-1 expression through the activation of the [[ extracellular signal-regulated kinase ]] (ERK).


Both << H(2)S >> solution prepared by bubbling pure H(2)S gas and NaSH, a H(2)S donor, dose dependently induced HO-1 expression through the activation of the extracellular signal-regulated kinase ([[ ERK ]]).


Both << H(2)S >> solution prepared by bubbling pure H(2)S gas and NaSH, a H(2)S donor, dose dependently induced [[ HO-1 ]] expression through the activation of the extracellular signal-regulated kinase (ERK).


Pretreatment with << H(2)S >> or NaHS significantly inhibited LPS-induced [[ iNOS ]] expression and NO production.


Pretreatment with H(2)S or << NaHS >> significantly inhibited LPS-induced [[ iNOS ]] expression and NO production.


Pretreatment with H(2)S or NaHS significantly inhibited LPS-induced << iNOS >> expression and [[ NO ]] production.


Moreover, NO production in LPS-stimulated macrophages that are expressing CSE mRNA was significantly reduced by the addition of L-Cys, a substrate for H(2)S, but enhanced by the selective << CSE >> inhibitor [[ beta-cyano-L-alanine ]] but not by the CBS inhibitor aminooxyacetic acid.


Moreover, NO production in LPS-stimulated macrophages that are expressing CSE mRNA was significantly reduced by the addition of L-Cys, a substrate for H(2)S, but enhanced by the selective CSE inhibitor beta-cyano-L-alanine but not by the << CBS >> inhibitor [[ aminooxyacetic acid ]].


Moreover, NO production in LPS-stimulated macrophages that are expressing << CSE >> mRNA was significantly reduced by the addition of [[ L-Cys ]], a substrate for H(2)S, but enhanced by the selective CSE inhibitor beta-cyano-L-alanine but not by the CBS inhibitor aminooxyacetic acid.


While either blockage of HO activity by the HO inhibitor, tin protoporphyrin IX, or down-regulation of HO-1 expression by HO-1 small interfering RNA (siRNA) reversed the inhibitory effects of << H(2)S >> on [[ iNOS ]] expression and NO production, HO-1 overexpression produced the same inhibitory effects of H(2)S.


While either blockage of HO activity by the HO inhibitor, tin protoporphyrin IX, or down-regulation of HO-1 expression by HO-1 small interfering RNA (siRNA) reversed the inhibitory effects of H(2)S on << iNOS >> expression and [[ NO ]] production, HO-1 overexpression produced the same inhibitory effects of H(2)S.


In addition, LPS-induced nuclear factor << (NF)-kappaB >> activation was diminished in RAW264.7 macrophages preincubated with [[ H(2)S ]].


Interestingly, the inhibitory effect of << H(2)S >> on [[ NF-kappaB ]] activation was reversed by the transient transfection with HO-1 siRNA, but was mimicked by either HO-1 gene transfection or treatment with carbon monoxide (CO), an end product of HO-1.


Interestingly, the inhibitory effect of H(2)S on NF-kappaB activation was reversed by the transient transfection with HO-1 siRNA, but was mimicked by either HO-1 gene transfection or treatment with << carbon monoxide >> (CO), an end product of [[ HO-1 ]].


Interestingly, the inhibitory effect of H(2)S on NF-kappaB activation was reversed by the transient transfection with HO-1 siRNA, but was mimicked by either HO-1 gene transfection or treatment with carbon monoxide (<< CO >>), an end product of [[ HO-1 ]].


<< CO >> treatment also inhibited LPS-induced NO production and [[ iNOS ]] expression via its inactivation of NF-kappaB.


<< CO >> treatment also inhibited LPS-induced NO production and iNOS expression via its inactivation of [[ NF-kappaB ]].


CO treatment also inhibited LPS-induced << NO >> production and [[ iNOS ]] expression via its inactivation of NF-kappaB.


Collectively, our results suggest that << H(2)S >> can inhibit NO production and [[ NF-kappaB ]] activation in LPS-stimulated macrophages through a mechanism that involves the action of HO-1/CO.


Collectively, our results suggest that H(2)S can inhibit NO production and NF-kappaB activation in LPS-stimulated macrophages through a mechanism that involves the action of << HO-1 >>/[[ CO ]].


Sources of << L-arg >> include dietary proteins and endogenous synthesis by [[ argininosuccinate synthetase ]] and argininosuccinate lyase.


Sources of << L-arg >> include dietary proteins and endogenous synthesis by argininosuccinate synthetase and [[ argininosuccinate lyase ]].


L-arg is converted to << urea >> by [[ arginase I ]] in the liver and arginase II in the kidney.


L-arg is converted to << urea >> by arginase I in the liver and [[ arginase II ]] in the kidney.


<< L-arg >> is converted to urea by [[ arginase I ]] in the liver and arginase II in the kidney.


<< L-arg >> is converted to urea by arginase I in the liver and [[ arginase II ]] in the kidney.


We hypothesized that preservation of plasma << L-arg >> in CRF may be, partly, due to downregulation/inhibition of [[ arginase ]].


However, in vitro experiments simulating a uremic milieu revealed a marked concentration-dependent inhibition of << arginase >> activity by [[ urea ]] in the tissue lysates.


CONCLUSIONS: Although CRF does not change the abundance or intrinsic properties of << arginase >>, the inherent rise in [[ urea ]] concentration inhibits its enzymatic activity.


However, several promising nonpeptide, << vasopressin receptor >> antagonists have been described; these agents are [[ VPA-985 ]] (lixivaptan), YM-087 (conivaptan), OPC-41061 (tolvaptan), and SR-121463.


However, several promising nonpeptide, << vasopressin receptor >> antagonists have been described; these agents are VPA-985 ([[ lixivaptan ]]), YM-087 (conivaptan), OPC-41061 (tolvaptan), and SR-121463.


However, several promising nonpeptide, << vasopressin receptor >> antagonists have been described; these agents are VPA-985 (lixivaptan), [[ YM-087 ]] (conivaptan), OPC-41061 (tolvaptan), and SR-121463.


However, several promising nonpeptide, << vasopressin receptor >> antagonists have been described; these agents are VPA-985 (lixivaptan), YM-087 ([[ conivaptan ]]), OPC-41061 (tolvaptan), and SR-121463.


However, several promising nonpeptide, << vasopressin receptor >> antagonists have been described; these agents are VPA-985 (lixivaptan), YM-087 (conivaptan), [[ OPC-41061 ]] (tolvaptan), and SR-121463.


However, several promising nonpeptide, << vasopressin receptor >> antagonists have been described; these agents are VPA-985 (lixivaptan), YM-087 (conivaptan), OPC-41061 ([[ tolvaptan ]]), and SR-121463.


However, several promising nonpeptide, << vasopressin receptor >> antagonists have been described; these agents are VPA-985 (lixivaptan), YM-087 (conivaptan), OPC-41061 (tolvaptan), and [[ SR-121463 ]].


Sedation and << histamine H1-receptor >> antagonism: studies in man with the enantiomers of chlorpheniramine and [[ dimethindene ]].


Sedation and << histamine H1-receptor >> antagonism: studies in man with the enantiomers of [[ chlorpheniramine ]] and dimethindene.


BG also showed a protective effect in the presence of a << DNA polymerase beta >> inhibitor ([[ cytosine arabinoside-3-phosphate ]], Ara-C), demonstrating that BG does not act through an anti-mutagenic mechanism of action involving DNA polymerase beta.


BG also showed a protective effect in the presence of a << DNA polymerase beta >> inhibitor (cytosine arabinoside-3-phosphate, [[ Ara-C ]]), demonstrating that BG does not act through an anti-mutagenic mechanism of action involving DNA polymerase beta.


Reduction of cerebral infarct size by the AT1-receptor blocker candesartan, the << HMG-CoA reductase >> inhibitor [[ rosuvastatin ]] and their combination.


Reduction of cerebral infarct size by the << AT1 >>-receptor blocker [[ candesartan ]], the HMG-CoA reductase inhibitor rosuvastatin and their combination.


Our purpose was to test the impact of single and/or combined treatment with the << AT(1) >>-receptor blocker [[ candesartan ]] and the HMG-CoA reductase inhibitor rosuvastatin on infarct size and neuroscore in transient cerebral ischemia in rats.


Our purpose was to test the impact of single and/or combined treatment with the AT(1)-receptor blocker candesartan and the << HMG-CoA reductase >> inhibitor [[ rosuvastatin ]] on infarct size and neuroscore in transient cerebral ischemia in rats.


Diacylglycerol (DAG) acts as an allosteric activator of protein kinase C (PKC) and is converted to << phosphatidic acid >> by [[ DAG kinase ]] (DGK).


Diacylglycerol (DAG) acts as an allosteric activator of protein kinase C (PKC) and is converted to << phosphatidic acid >> by DAG kinase ([[ DGK ]]).


<< Diacylglycerol >> (DAG) acts as an allosteric activator of protein kinase C (PKC) and is converted to phosphatidic acid by [[ DAG kinase ]] (DGK).


<< Diacylglycerol >> (DAG) acts as an allosteric activator of protein kinase C (PKC) and is converted to phosphatidic acid by DAG kinase ([[ DGK ]]).


Diacylglycerol (<< DAG >>) acts as an allosteric activator of protein kinase C (PKC) and is converted to phosphatidic acid by [[ DAG kinase ]] (DGK).


Diacylglycerol (<< DAG >>) acts as an allosteric activator of protein kinase C (PKC) and is converted to phosphatidic acid by DAG kinase ([[ DGK ]]).


Monoclonal antibody 25B1 generated against << diisopropyl phosphorofluoridate >> inhibited fetal [[ bovine serum acetylcholinesterase ]] has been extensively characterized with respect to its anticholinesterase properties.


Monoclonal antibody 25B1 appears to be directed against a conformational epitope located in close proximity to the catalytic center of the enzyme and was found to be most suitable for studying the stabilization of the active site of << acetylcholinesterase >> against denaturation by heat or [[ guanidine ]] following phosphorylation by organophosphorus anticholinesterase compounds.


The << sordarins >> group are protein synthesis inhibitors that work by blocking the function of [[ fungal translation elongation factor 2 ]].


Phospholipase C beta (PLC-beta)-coupled G protein-coupled receptor (GPCR) activities traditionally are assessed by measuring Ca2+ triggered by << D-myo-inositol 1,4,5-trisphosphate >> (IP3), a [[ PLC-beta ]] hydrolysis product, or by measuring the production of inositol phosphate using cumbersome radioactive assays.


Phospholipase C beta (PLC-beta)-coupled G protein-coupled receptor (GPCR) activities traditionally are assessed by measuring Ca2+ triggered by D-myo-inositol 1,4,5-trisphosphate (<< IP3 >>), a [[ PLC-beta ]] hydrolysis product, or by measuring the production of inositol phosphate using cumbersome radioactive assays.


Phospholipase C beta (PLC-beta)-coupled G protein-coupled receptor (GPCR) activities traditionally are assessed by measuring Ca2+ triggered by D-myo-inositol 1,4,5-trisphosphate (IP3), a << PLC-beta >> hydrolysis product, or by measuring the production of [[ inositol phosphate ]] using cumbersome radioactive assays.


It has been known for decades that << lithium chloride >> (LiCl) leads to D-myo-inositol 1-phosphate accumulation on [[ GPCR ]] activation by inhibiting inositol monophosphatase, the final enzyme of the IP3 metabolic cascade.


It has been known for decades that lithium chloride (<< LiCl >>) leads to D-myo-inositol 1-phosphate accumulation on [[ GPCR ]] activation by inhibiting inositol monophosphatase, the final enzyme of the IP3 metabolic cascade.


It has been known for decades that << lithium chloride >> (LiCl) leads to D-myo-inositol 1-phosphate accumulation on GPCR activation by inhibiting [[ inositol monophosphatase ]], the final enzyme of the IP3 metabolic cascade.


It has been known for decades that lithium chloride (<< LiCl >>) leads to D-myo-inositol 1-phosphate accumulation on GPCR activation by inhibiting [[ inositol monophosphatase ]], the final enzyme of the IP3 metabolic cascade.


It has been known for decades that lithium chloride (LiCl) leads to << D-myo-inositol 1-phosphate >> accumulation on GPCR activation by inhibiting [[ inositol monophosphatase ]], the final enzyme of the IP3 metabolic cascade.


It has been known for decades that lithium chloride (LiCl) leads to D-myo-inositol 1-phosphate accumulation on GPCR activation by inhibiting << inositol monophosphatase >>, the final enzyme of the [[ IP3 ]] metabolic cascade.


Once formed, the molecule can be converted to << glycine >> by [[ alanine-glyoxylate aminotransferase ]] (AGAT).


Once formed, the molecule can be converted to << glycine >> by alanine-glyoxylate aminotransferase ([[ AGAT ]]).


<< 11Beta-HSD1 >> activates cortisone to [[ cortisol ]] to facilitate glucocorticoid receptor (GR)-mediated action.


<< 11Beta-HSD1 >> activates [[ cortisone ]] to cortisol to facilitate glucocorticoid receptor (GR)-mediated action.


By contrast, 11beta-HSD2 plays a pivotal role in aldosterone target tissues where it catalyses the opposite reaction (i.e. inactivation of cortisol to cortisone) to prevent activation of the << mineralocorticoid receptor >> (MR) by [[ cortisol ]].


By contrast, 11beta-HSD2 plays a pivotal role in aldosterone target tissues where it catalyses the opposite reaction (i.e. inactivation of cortisol to cortisone) to prevent activation of the mineralocorticoid receptor (<< MR >>) by [[ cortisol ]].


By contrast, << 11beta-HSD2 >> plays a pivotal role in aldosterone target tissues where it catalyses the opposite reaction (i.e. inactivation of cortisol to [[ cortisone ]]) to prevent activation of the mineralocorticoid receptor (MR) by cortisol.


By contrast, << 11beta-HSD2 >> plays a pivotal role in aldosterone target tissues where it catalyses the opposite reaction (i.e. inactivation of [[ cortisol ]] to cortisone) to prevent activation of the mineralocorticoid receptor (MR) by cortisol.


Mutations in the 11beta-HSD2 gene cause a rare form of inherited hypertension, the syndrome of apparent mineralocorticoid excess (AME), in which << cortisol >> activates the [[ MR ]] resulting in severe hypertension and hypokalemia.


Ingestion of competitive inhibitors of << 11beta-HSD2 >> such as liquorice and [[ carbenoxolone ]] result in a similar but milder clinical phenotype.


Here we demonstrate that PPARgamma, turns on << retinoic acid >> synthesis by inducing the expression of retinol and retinal metabolizing enzymes such as [[ retinol dehydrogenase 10 ]] and retinaldehyde dehydrogenase type 2 (RALDH2).


Here we demonstrate that PPARgamma, turns on << retinoic acid >> synthesis by inducing the expression of retinol and retinal metabolizing enzymes such as retinol dehydrogenase 10 and [[ retinaldehyde dehydrogenase type 2 ]] (RALDH2).


Here we demonstrate that PPARgamma, turns on << retinoic acid >> synthesis by inducing the expression of retinol and retinal metabolizing enzymes such as retinol dehydrogenase 10 and retinaldehyde dehydrogenase type 2 ([[ RALDH2 ]]).


Here we demonstrate that PPARgamma, turns on retinoic acid synthesis by inducing the expression of << retinol >> and retinal metabolizing enzymes such as [[ retinol dehydrogenase 10 ]] and retinaldehyde dehydrogenase type 2 (RALDH2).


Here we demonstrate that PPARgamma, turns on retinoic acid synthesis by inducing the expression of << retinol >> and retinal metabolizing enzymes such as retinol dehydrogenase 10 and [[ retinaldehyde dehydrogenase type 2 ]] (RALDH2).


Here we demonstrate that PPARgamma, turns on retinoic acid synthesis by inducing the expression of << retinol >> and retinal metabolizing enzymes such as retinol dehydrogenase 10 and retinaldehyde dehydrogenase type 2 ([[ RALDH2 ]]).


Here we demonstrate that PPARgamma, turns on retinoic acid synthesis by inducing the expression of retinol and << retinal >> metabolizing enzymes such as [[ retinol dehydrogenase 10 ]] and retinaldehyde dehydrogenase type 2 (RALDH2).


Here we demonstrate that PPARgamma, turns on retinoic acid synthesis by inducing the expression of retinol and << retinal >> metabolizing enzymes such as retinol dehydrogenase 10 and [[ retinaldehyde dehydrogenase type 2 ]] (RALDH2).


Here we demonstrate that PPARgamma, turns on retinoic acid synthesis by inducing the expression of retinol and << retinal >> metabolizing enzymes such as retinol dehydrogenase 10 and retinaldehyde dehydrogenase type 2 ([[ RALDH2 ]]).


<< ATRA >> regulates gene expression via the activation of the [[ retinoic acid receptor (RAR)alpha ]] in human DCs, and RARalpha acutely regulates CD1d expression.


<< ATRA >> regulates gene expression via the activation of the retinoic acid receptor (RAR)alpha in human DCs, and [[ RARalpha ]] acutely regulates CD1d expression.


<< ATRA >> regulates gene expression via the activation of the retinoic acid receptor (RAR)alpha in human DCs, and RARalpha acutely regulates [[ CD1d ]] expression.


The << retinoic acid >>-induced elevated expression of [[ CD1d ]] is coupled to enhanced iNKT cell activation.


Furthermore, in vivo relevant lipids such as oxidized low-density lipoprotein can also elicit << retinoid >> signaling leading to [[ CD1d ]] up-regulation.


CONTEXT: << Ramelteon >> is a novel [[ MT1 ]] and MT2 melatonin receptor selective agonist recently approved for insomnia treatment.


CONTEXT: << Ramelteon >> is a novel MT1 and [[ MT2 melatonin receptor ]] selective agonist recently approved for insomnia treatment.


Late INa induced by the << VGSC >> long QT mutant R1623Q was reduced by [[ resveratrol ]] and quercetin.


Late INa induced by the VGSC long QT mutant << R1623Q >> was reduced by [[ resveratrol ]] and quercetin.


Late INa induced by the << VGSC >> long QT mutant R1623Q was reduced by resveratrol and [[ quercetin ]].


Late INa induced by the VGSC long QT mutant << R1623Q >> was reduced by resveratrol and [[ quercetin ]].


Enhancement of radiosensitivity by << topoisomerase II >> inhibitor, [[ amrubicin ]] and amrubicinol, in human lung adenocarcinoma A549 cells and kinetics of apoptosis and necrosis induction.


Enhancement of radiosensitivity by << topoisomerase II >> inhibitor, amrubicin and [[ amrubicinol ]], in human lung adenocarcinoma A549 cells and kinetics of apoptosis and necrosis induction.


Similar to << AMR >> and AMROH, adriamycin and etoposide (VP-16) are [[ DNA topoisomerase II ]] inhibitors.


Similar to AMR and << AMROH >>, adriamycin and etoposide (VP-16) are [[ DNA topoisomerase II ]] inhibitors.


Similar to AMR and AMROH, << adriamycin >> and etoposide (VP-16) are [[ DNA topoisomerase II ]] inhibitors.


Similar to AMR and AMROH, adriamycin and << etoposide >> (VP-16) are [[ DNA topoisomerase II ]] inhibitors.


Similar to AMR and AMROH, adriamycin and etoposide (<< VP-16 >>) are [[ DNA topoisomerase II ]] inhibitors.


Accumulated evidence in humans and animals shows that both << aspirin >> and H. pylori upregulate the expression of [[ cyclooxygenase (COX)-2 ]] both at mRNA and protein levels at the ulcer margin, but failed to influence significantly that of COX-1.


It was, therefore, proposed that H. pylori may in fact, antagonize, << aspirin >>-induced delay of ulcer healing due to suppression of acid secretion by the enhancement in PGE(2) possibly derived from [[ COX-2 ]] expression and activity and to the overexpression of growth factors such as TGF alpha and VEGF.


It was, therefore, proposed that H. pylori may in fact, antagonize, << aspirin >>-induced delay of ulcer healing due to suppression of acid secretion by the enhancement in PGE(2) possibly derived from COX-2 expression and activity and to the overexpression of growth factors such as [[ TGF alpha ]] and VEGF.


It was, therefore, proposed that H. pylori may in fact, antagonize, << aspirin >>-induced delay of ulcer healing due to suppression of acid secretion by the enhancement in PGE(2) possibly derived from COX-2 expression and activity and to the overexpression of growth factors such as TGF alpha and [[ VEGF ]].


It was, therefore, proposed that H. pylori may in fact, antagonize, aspirin-induced delay of ulcer healing due to suppression of acid secretion by the enhancement in << PGE(2) >> possibly derived from [[ COX-2 ]] expression and activity and to the overexpression of growth factors such as TGF alpha and VEGF.


<< Methylthioadenosine phosphorylase >> (MTAP) salvages purines by releasing [[ adenine ]] from methylthioadenosine and is often deleted in mesothelioma.


Methylthioadenosine phosphorylase (<< MTAP >>) salvages purines by releasing [[ adenine ]] from methylthioadenosine and is often deleted in mesothelioma.


<< Methylthioadenosine phosphorylase >> (MTAP) salvages purines by releasing adenine from [[ methylthioadenosine ]] and is often deleted in mesothelioma.


Methylthioadenosine phosphorylase (<< MTAP >>) salvages purines by releasing adenine from [[ methylthioadenosine ]] and is often deleted in mesothelioma.


Based on selective nucleoside protection, TS was found to be the primary pemetrexed target in both cell lines with << GARFT >> inhibition requiring 20- to 30-fold higher [[ pemetrexed ]] concentrations.


Most drugs currently employed in the treatment of type 2 diabetes either target the sulfonylurea receptor stimulating << insulin >> release ([[ sulfonylureas ]], glinides), or target the peroxisome proliferator-activated receptor (PPARgamma) improving insulin resistance (thiazolidinediones).


Most drugs currently employed in the treatment of type 2 diabetes either target the sulfonylurea receptor stimulating << insulin >> release (sulfonylureas, [[ glinides ]]), or target the peroxisome proliferator-activated receptor (PPARgamma) improving insulin resistance (thiazolidinediones).


Our work shows that << sulfonylureas >> and glinides additionally bind to PPARgamma and exhibit [[ PPARgamma ]] agonistic activity.


Our work shows that sulfonylureas and << glinides >> additionally bind to PPARgamma and exhibit [[ PPARgamma ]] agonistic activity.


Among the measured compounds, << gliquidone >> and glipizide (two sulfonylureas), as well as nateglinide (a glinide), exhibit [[ PPARgamma ]] agonistic activity at concentrations comparable with those reached under pharmacological treatment.


Among the measured compounds, gliquidone and << glipizide >> (two sulfonylureas), as well as nateglinide (a glinide), exhibit [[ PPARgamma ]] agonistic activity at concentrations comparable with those reached under pharmacological treatment.


Among the measured compounds, gliquidone and glipizide (two << sulfonylureas >>), as well as nateglinide (a glinide), exhibit [[ PPARgamma ]] agonistic activity at concentrations comparable with those reached under pharmacological treatment.


Among the measured compounds, gliquidone and glipizide (two sulfonylureas), as well as << nateglinide >> (a glinide), exhibit [[ PPARgamma ]] agonistic activity at concentrations comparable with those reached under pharmacological treatment.


Among the measured compounds, gliquidone and glipizide (two sulfonylureas), as well as nateglinide (a << glinide >>), exhibit [[ PPARgamma ]] agonistic activity at concentrations comparable with those reached under pharmacological treatment.


The most active of these compounds, << gliquidone >>, is shown to be as potent as pioglitazone at inducing [[ PPARgamma ]] target gene expression.


The most active of these compounds, gliquidone, is shown to be as potent as << pioglitazone >> at inducing [[ PPARgamma ]] target gene expression.


<< Glinides >>, sulfonylureas, and other acidified sulfonamides may be promising leads in the development of new [[ PPARgamma ]] agonists.


Glinides, << sulfonylureas >>, and other acidified sulfonamides may be promising leads in the development of new [[ PPARgamma ]] agonists.


Glinides, sulfonylureas, and other << acidified sulfonamides >> may be promising leads in the development of new [[ PPARgamma ]] agonists.


Such organization results in the local activation of << PKA >> subsets through the generation of confined intracellular gradients of [[ cAMP ]], but the mechanisms responsible for limiting the diffusion of cAMP largely remain to be clarified.


By using pharmacological and genetic manipulation of phosphodiesterases (PDEs), we demonstrate that compartmentalized << PDE4B >> and PDE4D are responsible for selectively modulating the concentration of [[ cAMP ]] in individual subcellular compartments.


By using pharmacological and genetic manipulation of phosphodiesterases (PDEs), we demonstrate that compartmentalized PDE4B and << PDE4D >> are responsible for selectively modulating the concentration of [[ cAMP ]] in individual subcellular compartments.


We propose a model whereby compartmentalized << PDEs >>, rather than representing an enzymatic barrier to cAMP diffusion, act as a sink to drain the second messenger from discrete locations, resulting in multiple and simultaneous domains with different [[ cAMP ]] concentrations irrespective of their distance from the site of cAMP synthesis.


We propose a model whereby compartmentalized << PDEs >>, rather than representing an enzymatic barrier to cAMP diffusion, act as a sink to drain the second messenger from discrete locations, resulting in multiple and simultaneous domains with different cAMP concentrations irrespective of their distance from the site of [[ cAMP ]] synthesis.


SK-Br3 cells cultured in the presence of topoisomerase IIalpha (TOP2A) inhibitors << doxorubicin >> and etopoxide (VP-16) demonstrated a 2- to 3-fold increase in [[ FAS promoter ]] activity when compared with control cells growing in drug-free culture conditions.


SK-Br3 cells cultured in the presence of topoisomerase IIalpha (TOP2A) inhibitors doxorubicin and << etopoxide >> (VP-16) demonstrated a 2- to 3-fold increase in [[ FAS promoter ]] activity when compared with control cells growing in drug-free culture conditions.


SK-Br3 cells cultured in the presence of topoisomerase IIalpha (TOP2A) inhibitors doxorubicin and etopoxide (<< VP-16 >>) demonstrated a 2- to 3-fold increase in [[ FAS promoter ]] activity when compared with control cells growing in drug-free culture conditions.


SK-Br3 cells cultured in the presence of << topoisomerase IIalpha >> (TOP2A) inhibitors [[ doxorubicin ]] and etopoxide (VP-16) demonstrated a 2- to 3-fold increase in FAS promoter activity when compared with control cells growing in drug-free culture conditions.


SK-Br3 cells cultured in the presence of topoisomerase IIalpha (<< TOP2A >>) inhibitors [[ doxorubicin ]] and etopoxide (VP-16) demonstrated a 2- to 3-fold increase in FAS promoter activity when compared with control cells growing in drug-free culture conditions.


SK-Br3 cells cultured in the presence of << topoisomerase IIalpha >> (TOP2A) inhibitors doxorubicin and [[ etopoxide ]] (VP-16) demonstrated a 2- to 3-fold increase in FAS promoter activity when compared with control cells growing in drug-free culture conditions.


SK-Br3 cells cultured in the presence of topoisomerase IIalpha (<< TOP2A >>) inhibitors doxorubicin and [[ etopoxide ]] (VP-16) demonstrated a 2- to 3-fold increase in FAS promoter activity when compared with control cells growing in drug-free culture conditions.


SK-Br3 cells cultured in the presence of << topoisomerase IIalpha >> (TOP2A) inhibitors doxorubicin and etopoxide ([[ VP-16 ]]) demonstrated a 2- to 3-fold increase in FAS promoter activity when compared with control cells growing in drug-free culture conditions.


SK-Br3 cells cultured in the presence of topoisomerase IIalpha (<< TOP2A >>) inhibitors doxorubicin and etopoxide ([[ VP-16 ]]) demonstrated a 2- to 3-fold increase in FAS promoter activity when compared with control cells growing in drug-free culture conditions.


RESULT(S): The expression of endometrial << ERalpha >>, PRAB, PRB, and SRC-1 was increased significantly after 1 week of [[ mifepristone ]], but the increase was no longer seen after 10 weeks.


RESULT(S): The expression of endometrial ERalpha, << PRAB >>, PRB, and SRC-1 was increased significantly after 1 week of [[ mifepristone ]], but the increase was no longer seen after 10 weeks.


RESULT(S): The expression of endometrial ERalpha, PRAB, << PRB >>, and SRC-1 was increased significantly after 1 week of [[ mifepristone ]], but the increase was no longer seen after 10 weeks.


RESULT(S): The expression of endometrial ERalpha, PRAB, PRB, and << SRC-1 >> was increased significantly after 1 week of [[ mifepristone ]], but the increase was no longer seen after 10 weeks.


CONCLUSION(S): Short-term exposure of << mifepristone >> in new starters of DMPA increases the expression of endometrial [[ ERalpha ]], PRAB, PRB, and SRC-1 and promotes cell proliferation.


CONCLUSION(S): Short-term exposure of << mifepristone >> in new starters of DMPA increases the expression of endometrial ERalpha, [[ PRAB ]], PRB, and SRC-1 and promotes cell proliferation.


CONCLUSION(S): Short-term exposure of << mifepristone >> in new starters of DMPA increases the expression of endometrial ERalpha, PRAB, [[ PRB ]], and SRC-1 and promotes cell proliferation.


CONCLUSION(S): Short-term exposure of << mifepristone >> in new starters of DMPA increases the expression of endometrial ERalpha, PRAB, PRB, and [[ SRC-1 ]] and promotes cell proliferation.


In the present study, << glucose >>-stimulated [[ insulin ]] secretion was significantly increased in GalN-treated rats compared to controls.


In the present study, glucose-stimulated << insulin >> secretion was significantly increased in [[ GalN ]]-treated rats compared to controls.


Levels of mRNA encoding << insulin 1 >>, ICA512, and PC1/3 were increased in the pancreatic islets of [[ GalN ]]-treated rats.


Levels of mRNA encoding insulin 1, << ICA512 >>, and PC1/3 were increased in the pancreatic islets of [[ GalN ]]-treated rats.


When the << PTB-binding site >> in insulin 1 mRNA was incubated with the islet cytosolic fraction, the RNA-protein complex level was increased in the cytosolic fraction obtained from [[ GalN ]]-treated rats compared to the level in control rats.


When the PTB-binding site in << insulin 1 >> mRNA was incubated with the islet cytosolic fraction, the RNA-protein complex level was increased in the cytosolic fraction obtained from [[ GalN ]]-treated rats compared to the level in control rats.


The cytosolic fraction obtained from pancreatic islets obtained from << GalN >>-treated rats had an increased [[ PTB ]] level compared to the levels obtained from the pancreatic islets of control rats.


The changes in CysLT1 receptor expression 24 h after NMDA injection and the effects of a << CysLT1 receptor >> antagonist, [[ pranlukast ]] (0.01 and 0.1 mg/kg), an NMDA receptor antagonist, ketamine (30 mg/kg), and an antioxidant, edaravone (9 mg/kg) were observed.


The changes in CysLT1 receptor expression 24 h after NMDA injection and the effects of a CysLT1 receptor antagonist, pranlukast (0.01 and 0.1 mg/kg), an << NMDA receptor >> antagonist, [[ ketamine ]] (30 mg/kg), and an antioxidant, edaravone (9 mg/kg) were observed.


RESULTS: In the << NMDA >>-injured brain, the [[ CysLT1 receptor ]] mRNA, and protein expression were upregulated, and the receptor was mainly localized in the neurons and not in the astrocytes.


Pranlukast, ketamine and edaravone decreased NMDA-induced injury; << pranlukast >> (0.1 mg/kg) and ketamine inhibited the upregulated expression of the [[ CysLT1 receptor ]].


Pranlukast, ketamine and edaravone decreased NMDA-induced injury; pranlukast (0.1 mg/kg) and << ketamine >> inhibited the upregulated expression of the [[ CysLT1 receptor ]].


CONCLUSION: << CysLT1 receptor >> expression in neurons is upregulated after [[ NMDA ]] injection, and NMDA-induced responses are inhibited by CysLT1 receptor antagonists, indicating that the increased CysLT1 receptor is involved in NMDA excitotoxicity.


CONCLUSION: CysLT1 receptor expression in neurons is upregulated after NMDA injection, and NMDA-induced responses are inhibited by CysLT1 receptor antagonists, indicating that the increased << CysLT1 receptor >> is involved in [[ NMDA ]] excitotoxicity.


We have previously demonstrated that phosphorylation of << Fas-associated death domain-containing protein >> (FADD) at 194 serine through c-jun NH2-terminal kinase (JNK) activation sensitizes breast cancer cells to chemotherapy through accelerating cell cycle arrest at G2/M, and that Bcl-2 phosphorylation downstream of JNK/FADD plays an important role in cell growth suppression by [[ paclitaxel ]].


We have previously demonstrated that phosphorylation of Fas-associated death domain-containing protein (<< FADD >>) at 194 serine through c-jun NH2-terminal kinase (JNK) activation sensitizes breast cancer cells to chemotherapy through accelerating cell cycle arrest at G2/M, and that Bcl-2 phosphorylation downstream of JNK/FADD plays an important role in cell growth suppression by [[ paclitaxel ]].


We have previously demonstrated that phosphorylation of Fas-associated death domain-containing protein (FADD) at 194 serine through << c-jun NH2-terminal kinase >> (JNK) activation sensitizes breast cancer cells to chemotherapy through accelerating cell cycle arrest at G2/M, and that Bcl-2 phosphorylation downstream of JNK/FADD plays an important role in cell growth suppression by [[ paclitaxel ]].


We have previously demonstrated that phosphorylation of Fas-associated death domain-containing protein (FADD) at 194 serine through c-jun NH2-terminal kinase (<< JNK >>) activation sensitizes breast cancer cells to chemotherapy through accelerating cell cycle arrest at G2/M, and that Bcl-2 phosphorylation downstream of JNK/FADD plays an important role in cell growth suppression by [[ paclitaxel ]].


We have previously demonstrated that phosphorylation of Fas-associated death domain-containing protein (FADD) at 194 serine through c-jun NH2-terminal kinase (JNK) activation sensitizes breast cancer cells to chemotherapy through accelerating cell cycle arrest at G2/M, and that Bcl-2 phosphorylation downstream of << JNK >>/FADD plays an important role in cell growth suppression by [[ paclitaxel ]].


We have previously demonstrated that phosphorylation of Fas-associated death domain-containing protein (FADD) at 194 serine through c-jun NH2-terminal kinase (JNK) activation sensitizes breast cancer cells to chemotherapy through accelerating cell cycle arrest at G2/M, and that Bcl-2 phosphorylation downstream of JNK/<< FADD >> plays an important role in cell growth suppression by [[ paclitaxel ]].


The mechanism(s) responsible for arterial vasodilation observed following acute administration of << racemic carvedilol >>, a novel vasodilator/[[ beta adrenoceptor ]] antagonist, has been investigated in rats.


Carvedilol (0.3 mg/kg, iv) produced a significant inhibition of the << beta 1 adrenoceptor >> mediated positive chronotropic response to [[ isoproterenol ]].


<< Carvedilol >> (0.3 mg/kg, iv) produced a significant inhibition of the [[ beta 1 adrenoceptor ]] mediated positive chronotropic response to isoproterenol.


This same dose of << carvedilol >> also inhibited, but to a lesser degree, the [[ beta 2 adrenoceptor ]] mediated vasodepressor response to salbutamol in pithed rats whose blood pressure was elevated by a constant intravenous infusion of angiotensin II.


Thus, << carvedilol >> blocks both beta 1 and beta 2 adrenoceptors at antihypertensive doses, with modest selectivity being observed for the [[ beta 1 adrenoceptor ]] subtype.


<< Carvedilol >> produced significant inhibition of the [[ alpha 1 adrenoceptor ]] mediated pressor response to cirazoline in the pithed rat, but had no effect on the alpha 2 adrenoceptor mediated pressor response to B-HT 933, suggesting that carvedilol is also an alpha 1 adrenoceptor antagonist at antihypertensive doses.


Carvedilol produced significant inhibition of the alpha 1 adrenoceptor mediated pressor response to cirazoline in the pithed rat, but had no effect on the alpha 2 adrenoceptor mediated pressor response to B-HT 933, suggesting that << carvedilol >> is also an [[ alpha 1 adrenoceptor ]] antagonist at antihypertensive doses.


The vasopressor response to the << calcium channel >> activator, [[ BAY-K-8644 ]], which is mediated through the opening of voltage dependent calcium channels and the subsequent translocation of extracellular calcium, was significantly inhibited by carvedilol (1 mg/kg, iv), suggesting that carvedilol is also a calcium channel antagonist, consistent with our previous in vitro studies.


The vasopressor response to the calcium channel activator, << BAY-K-8644 >>, which is mediated through the opening of [[ voltage dependent calcium channels ]] and the subsequent translocation of extracellular calcium, was significantly inhibited by carvedilol (1 mg/kg, iv), suggesting that carvedilol is also a calcium channel antagonist, consistent with our previous in vitro studies.


The vasopressor response to the calcium channel activator, BAY-K-8644, which is mediated through the opening of << voltage dependent calcium channels >> and the subsequent translocation of extracellular calcium, was significantly inhibited by [[ carvedilol ]] (1 mg/kg, iv), suggesting that carvedilol is also a calcium channel antagonist, consistent with our previous in vitro studies.


The vasopressor response to the calcium channel activator, BAY-K-8644, which is mediated through the opening of voltage dependent calcium channels and the subsequent translocation of extracellular calcium, was significantly inhibited by carvedilol (1 mg/kg, iv), suggesting that << carvedilol >> is also a [[ calcium channel ]] antagonist, consistent with our previous in vitro studies.


The vasopressor response to the calcium channel activator, BAY-K-8644, which is mediated through the opening of << voltage dependent calcium channels >> and the subsequent translocation of extracellular [[ calcium ]], was significantly inhibited by carvedilol (1 mg/kg, iv), suggesting that carvedilol is also a calcium channel antagonist, consistent with our previous in vitro studies.


In anesthetized spontaneously hypertensive rats, the antihypertensive activity of carvedilol was nearly abolished by combined pretreatment of the rats with high doses of the << alpha 1 adrenoceptor >> antagonist, [[ prazosin ]] (1 mg/kg, iv), and the nonselective beta adrenoceptor antagonist, propranolol (3 mg/kg, iv), suggesting that the majority of the antihypertensive response produced by carvedilol may be accounted for by blockade of beta and alpha 1 adrenoceptors.


In anesthetized spontaneously hypertensive rats, the antihypertensive activity of carvedilol was nearly abolished by combined pretreatment of the rats with high doses of the alpha 1 adrenoceptor antagonist, prazosin (1 mg/kg, iv), and the nonselective << beta adrenoceptor >> antagonist, [[ propranolol ]] (3 mg/kg, iv), suggesting that the majority of the antihypertensive response produced by carvedilol may be accounted for by blockade of beta and alpha 1 adrenoceptors.


We therefore conclude that << carvedilol >>, at antihypertensive doses, is an antagonist of beta 1, beta 2, and alpha 1 adrenoceptors, and also of [[ calcium channels ]] in vascular smooth muscle.(ABSTRACT TRUNCATED AT 400 WORDS)


<< 5-HT3 receptor >> antagonism with [[ alosetron ]] reduced responses to 5-HT in controls but not during inflammation.


<< Progestin >> activation of [[ Src ]]/MAPK occurred outside the nucleus with the B isoform of PR that was distributed between the cytoplasm and nucleus, but not with PR-A that was predominantly nuclear.


<< Progestin >> activation of Src/[[ MAPK ]] occurred outside the nucleus with the B isoform of PR that was distributed between the cytoplasm and nucleus, but not with PR-A that was predominantly nuclear.


<< Progestin >> induction of the cyclin D1 gene, which lacks a progesterone response element, was dependent on [[ PR ]] activation of the Src/MAPK pathway, whereas induction of the Sgk (serum and glucocorticoid regulated kinase) gene that contains a functional progesterone response element was unaffected by mutations that interfere with PR activation of Src.


<< Progestin >> induction of the cyclin D1 gene, which lacks a progesterone response element, was dependent on PR activation of the [[ Src ]]/MAPK pathway, whereas induction of the Sgk (serum and glucocorticoid regulated kinase) gene that contains a functional progesterone response element was unaffected by mutations that interfere with PR activation of Src.


<< Progestin >> induction of the cyclin D1 gene, which lacks a progesterone response element, was dependent on PR activation of the Src/[[ MAPK ]] pathway, whereas induction of the Sgk (serum and glucocorticoid regulated kinase) gene that contains a functional progesterone response element was unaffected by mutations that interfere with PR activation of Src.


These results highlight the importance of << PR >> activation of the Src/MAPK signaling pathway for [[ progesterone ]]-induced transcription of select target genes and cell cycle progression.


These results highlight the importance of PR activation of the << Src >>/MAPK signaling pathway for [[ progesterone ]]-induced transcription of select target genes and cell cycle progression.


These results highlight the importance of PR activation of the Src/<< MAPK >> signaling pathway for [[ progesterone ]]-induced transcription of select target genes and cell cycle progression.


i.p. injection of a subthreshold dose of << picrotoxin >>, a use-dependent [[ gamma-aminobutyric acid receptor ]] antagonist, reduces cortical electroencephalogram delta power and transiently inhibits spontaneous seizure activity in ADNFLE mutant mice.


MicroPET imaging in nonhuman primates with [<< 11C >>]1 and [11C]2 demonstrated that both tracers behave similarly in vivo with high uptake being observed in the [[ SERT ]]-rich brain regions and peak uptake being achieved in about 55 min postinjection.


MicroPET imaging in nonhuman primates with [11C]1 and [<< 11C >>]2 demonstrated that both tracers behave similarly in vivo with high uptake being observed in the [[ SERT ]]-rich brain regions and peak uptake being achieved in about 55 min postinjection.


This trial investigated the possibility of pharmacokinetic interactions between the << AT1 receptor >> antagonist [[ olmesartan medoxomil ]] and the thiazide diuretic hydrochlorothiazide in healthy subjects.


<< SecS >> required selenophosphate and O-phosphoseryl-tRNA([Ser]Sec) as substrates to generate [[ selenocysteyl ]]-tRNA([Ser]Sec).


<< SecS >> required selenophosphate and [[ O-phosphoseryl ]]-tRNA([Ser]Sec) as substrates to generate selenocysteyl-tRNA([Ser]Sec).


<< SecS >> required [[ selenophosphate ]] and O-phosphoseryl-tRNA([Ser]Sec) as substrates to generate selenocysteyl-tRNA([Ser]Sec).


In addition, we found that << selenophosphate synthetase 2 >> could synthesize [[ monoselenophosphate ]] in vitro but selenophosphate synthetase 1 could not.


<< Triflusal >> (30 mg/kg) also significantly decreased the protein levels of [[ IL-Ibeta ]] but not nuclear factor kappa B or tumor necrosis factor-alpha in the cortex ipsilateral to the middle cerebral artery occlusion.


<< Glutamate >> stimulates [[ glutamate receptor interacting protein 1 ]] degradation by ubiquitin-proteasome system to regulate surface expression of GluR2.


Here we report that << glutamate >> stimulation caused a rapid reduction in protein levels of [[ GRIP1 ]], but not that of glutamate receptor (GluR) 1, GluR2 and protein interacting with C kinase 1 (PICK1) in rat primary cortical neuron cultures.


Down-regulation of << GRIP1 >> by [[ glutamate ]] was blocked by carbobenzoxyl-leucinyl-leucinyl-leucinal (MG132), a proteasome inhibitor and by expression of K48R-ubiquitin, a dominant negative form of ubiquitin.


Down-regulation of GRIP1 by glutamate was blocked by carbobenzoxyl-leucinyl-leucinyl-leucinal (<< MG132 >>), a [[ proteasome ]] inhibitor and by expression of K48R-ubiquitin, a dominant negative form of ubiquitin.


Down-regulation of GRIP1 by glutamate was blocked by << carbobenzoxyl-leucinyl-leucinyl-leucinal >> (MG132), a [[ proteasome ]] inhibitor and by expression of K48R-ubiquitin, a dominant negative form of ubiquitin.


The << GRIP1 >> reduction was inhibited by [[ MK-801 ]], an N-methyl-d-aspartate (NMDA) receptor antagonist, but not by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), an AMPA receptor antagonist.


The GRIP1 reduction was inhibited by << MK-801 >>, an [[ N-methyl-d-aspartate (NMDA) receptor ]] antagonist, but not by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), an AMPA receptor antagonist.


The GRIP1 reduction was inhibited by MK-801, an N-methyl-d-aspartate (NMDA) receptor antagonist, but not by << 6-cyano-7-nitroquinoxaline-2,3-dione >> (CNQX), an [[ AMPA receptor ]] antagonist.


The GRIP1 reduction was inhibited by MK-801, an N-methyl-d-aspartate (NMDA) receptor antagonist, but not by 6-cyano-7-nitroquinoxaline-2,3-dione (<< CNQX >>), an [[ AMPA receptor ]] antagonist.


<< EGTA >> and 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetra acetic acid tetrakis (BAPTA), two Ca2+ chelators, but not nifedipine, an L-type Ca2+ channel blocker, prevented [[ GRIP1 ]] degradation.


EGTA and << 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetra acetic acid tetrakis >> (BAPTA), two Ca2+ chelators, but not nifedipine, an L-type Ca2+ channel blocker, prevented [[ GRIP1 ]] degradation.


EGTA and 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetra acetic acid tetrakis (<< BAPTA >>), two Ca2+ chelators, but not nifedipine, an L-type Ca2+ channel blocker, prevented [[ GRIP1 ]] degradation.


EGTA and 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetra acetic acid tetrakis (BAPTA), two Ca2+ chelators, but not << nifedipine >>, an [[ L-type Ca2+ channel ]] blocker, prevented GRIP1 degradation.


Furthermore, MG132 prevented << glutamate >>-stimulated reduction in surface amount of [[ GluR2 ]], and knockdown of GRIP1 by RNAi against GRIP1 reduced surface GluR2 in neurons.


Our results suggest that << glutamate >> induces [[ GRIP1 ]] degradation by proteasome through an NMDA receptor-Ca2+ pathway and that GRIP1 degradation may play an important role in regulating GluR2 surface expression.


Our results suggest that << glutamate >> induces GRIP1 degradation by proteasome through an NMDA receptor-Ca2+ pathway and that [[ GRIP1 ]] degradation may play an important role in regulating GluR2 surface expression.


The inhibitory effect of the leukotriene receptor antagonist on << leukotriene D4 >>-induced MUC2/5AC gene expression and [[ mucin ]] secretion in human airway epithelial cells.


The inhibitory effect of the leukotriene receptor antagonist on << leukotriene D4 >>-induced [[ MUC2/5AC ]] gene expression and mucin secretion in human airway epithelial cells.