<< Epidermal growth factor receptor >> inhibitors currently under investigation include the small molecules [[ gefitinib ]] (Iressa, ZD1839) and erlotinib (Tarceva, OSI-774), as well as monoclonal antibodies such as cetuximab (IMC-225, Erbitux).


<< Epidermal growth factor receptor >> inhibitors currently under investigation include the small molecules gefitinib ([[ Iressa ]], ZD1839) and erlotinib (Tarceva, OSI-774), as well as monoclonal antibodies such as cetuximab (IMC-225, Erbitux).


<< Epidermal growth factor receptor >> inhibitors currently under investigation include the small molecules gefitinib (Iressa, [[ ZD1839 ]]) and erlotinib (Tarceva, OSI-774), as well as monoclonal antibodies such as cetuximab (IMC-225, Erbitux).


<< Epidermal growth factor receptor >> inhibitors currently under investigation include the small molecules gefitinib (Iressa, ZD1839) and [[ erlotinib ]] (Tarceva, OSI-774), as well as monoclonal antibodies such as cetuximab (IMC-225, Erbitux).


<< Epidermal growth factor receptor >> inhibitors currently under investigation include the small molecules gefitinib (Iressa, ZD1839) and erlotinib ([[ Tarceva ]], OSI-774), as well as monoclonal antibodies such as cetuximab (IMC-225, Erbitux).


<< Epidermal growth factor receptor >> inhibitors currently under investigation include the small molecules gefitinib (Iressa, ZD1839) and erlotinib (Tarceva, [[ OSI-774 ]]), as well as monoclonal antibodies such as cetuximab (IMC-225, Erbitux).


<< Epidermal growth factor receptor >> inhibitors currently under investigation include the small molecules gefitinib (Iressa, ZD1839) and erlotinib (Tarceva, OSI-774), as well as monoclonal antibodies such as [[ cetuximab ]] (IMC-225, Erbitux).


<< Epidermal growth factor receptor >> inhibitors currently under investigation include the small molecules gefitinib (Iressa, ZD1839) and erlotinib (Tarceva, OSI-774), as well as monoclonal antibodies such as cetuximab ([[ IMC-225 ]], Erbitux).


<< Epidermal growth factor receptor >> inhibitors currently under investigation include the small molecules gefitinib (Iressa, ZD1839) and erlotinib (Tarceva, OSI-774), as well as monoclonal antibodies such as cetuximab (IMC-225, [[ Erbitux ]]).


Agents that have only begun to undergo clinical evaluation include << CI-1033 >>, an irreversible pan-[[ erbB ]] tyrosine kinase inhibitor, and PKI166 and GW572016, both examples of dual kinase inhibitors (inhibiting epidermal growth factor receptor and Her2).


Agents that have only begun to undergo clinical evaluation include << CI-1033 >>, an irreversible pan-erbB [[ tyrosine kinase ]] inhibitor, and PKI166 and GW572016, both examples of dual kinase inhibitors (inhibiting epidermal growth factor receptor and Her2).


Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-erbB tyrosine kinase inhibitor, and << PKI166 >> and GW572016, both examples of dual [[ kinase ]] inhibitors (inhibiting epidermal growth factor receptor and Her2).


Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-erbB tyrosine kinase inhibitor, and << PKI166 >> and GW572016, both examples of dual kinase inhibitors (inhibiting [[ epidermal growth factor receptor ]] and Her2).


Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-erbB tyrosine kinase inhibitor, and << PKI166 >> and GW572016, both examples of dual kinase inhibitors (inhibiting epidermal growth factor receptor and [[ Her2 ]]).


Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-erbB tyrosine kinase inhibitor, and PKI166 and << GW572016 >>, both examples of dual [[ kinase ]] inhibitors (inhibiting epidermal growth factor receptor and Her2).


Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-erbB tyrosine kinase inhibitor, and PKI166 and << GW572016 >>, both examples of dual kinase inhibitors (inhibiting [[ epidermal growth factor receptor ]] and Her2).


Agents that have only begun to undergo clinical evaluation include CI-1033, an irreversible pan-erbB tyrosine kinase inhibitor, and PKI166 and << GW572016 >>, both examples of dual kinase inhibitors (inhibiting epidermal growth factor receptor and [[ Her2 ]]).


<< Alprenolol >> and bromoacetylalprenololmenthane are competitive slowly reversible antagonists at the [[ beta 1-adrenoceptors ]] of rat left atria.


Alprenolol and << bromoacetylalprenololmenthane >> are competitive slowly reversible antagonists at the [[ beta 1-adrenoceptors ]] of rat left atria.


<< Alprenolol >> and BAAM at 10(-7), 3 x 10(-7), and 10(-6) M inhibited the cardiac stimulation response slightly, which is indicative of membrane-stabilizing activity independent of [[ beta-adrenoceptor ]] blockade.


Alprenolol and << BAAM >> at 10(-7), 3 x 10(-7), and 10(-6) M inhibited the cardiac stimulation response slightly, which is indicative of membrane-stabilizing activity independent of [[ beta-adrenoceptor ]] blockade.


Alprenolol and BAAM also caused surmountable antagonism of << isoprenaline >> responses, and this [[ beta 1-adrenoceptor ]] antagonism was slowly reversible.


<< Alprenolol >> and BAAM also caused surmountable antagonism of isoprenaline responses, and this [[ beta 1-adrenoceptor ]] antagonism was slowly reversible.


Alprenolol and << BAAM >> also caused surmountable antagonism of isoprenaline responses, and this [[ beta 1-adrenoceptor ]] antagonism was slowly reversible.


We conclude that << alprenolol >> and BAAM are competitive slowly reversible [[ beta 1-adrenoceptor ]] antagonists on rat left atria.


We conclude that alprenolol and << BAAM >> are competitive slowly reversible [[ beta 1-adrenoceptor ]] antagonists on rat left atria.


Discovery and optimization of << anthranilic acid sulfonamides >> as inhibitors of methionine aminopeptidase-2: a structural basis for the reduction of [[ albumin ]] binding.


<< Adenine phosphoribosyltransferase >> plays a role in purine salvage by catalyzing the direct conversion of adenine to [[ adenosine monophosphate ]].


<< Adenine phosphoribosyltransferase >> plays a role in purine salvage by catalyzing the direct conversion of [[ adenine ]] to adenosine monophosphate.


BACKGROUND: Since the introduction of the first << cholinesterase >> inhibitor (ChEI) in 1997, most clinicians and probably most patients would consider the cholinergic drugs, [[ donepezil ]], galantamine and rivastigmine, to be the first line pharmacotherapy for mild to moderate Alzheimer's disease.The drugs have slightly different pharmacological properties, but they all work by inhibiting the breakdown of acetylcholine, an important neurotransmitter associated with memory, by blocking the enzyme acetylcholinesterase.


BACKGROUND: Since the introduction of the first cholinesterase inhibitor (ChEI) in 1997, most clinicians and probably most patients would consider the cholinergic drugs, << donepezil >>, galantamine and rivastigmine, to be the first line pharmacotherapy for mild to moderate Alzheimer's disease.The drugs have slightly different pharmacological properties, but they all work by inhibiting the breakdown of acetylcholine, an important neurotransmitter associated with memory, by blocking the enzyme [[ acetylcholinesterase ]].


BACKGROUND: Since the introduction of the first << cholinesterase >> inhibitor (ChEI) in 1997, most clinicians and probably most patients would consider the cholinergic drugs, donepezil, [[ galantamine ]] and rivastigmine, to be the first line pharmacotherapy for mild to moderate Alzheimer's disease.The drugs have slightly different pharmacological properties, but they all work by inhibiting the breakdown of acetylcholine, an important neurotransmitter associated with memory, by blocking the enzyme acetylcholinesterase.


BACKGROUND: Since the introduction of the first cholinesterase inhibitor (ChEI) in 1997, most clinicians and probably most patients would consider the cholinergic drugs, donepezil, << galantamine >> and rivastigmine, to be the first line pharmacotherapy for mild to moderate Alzheimer's disease.The drugs have slightly different pharmacological properties, but they all work by inhibiting the breakdown of acetylcholine, an important neurotransmitter associated with memory, by blocking the enzyme [[ acetylcholinesterase ]].


BACKGROUND: Since the introduction of the first << cholinesterase >> inhibitor (ChEI) in 1997, most clinicians and probably most patients would consider the cholinergic drugs, donepezil, galantamine and [[ rivastigmine ]], to be the first line pharmacotherapy for mild to moderate Alzheimer's disease.The drugs have slightly different pharmacological properties, but they all work by inhibiting the breakdown of acetylcholine, an important neurotransmitter associated with memory, by blocking the enzyme acetylcholinesterase.


BACKGROUND: Since the introduction of the first cholinesterase inhibitor (ChEI) in 1997, most clinicians and probably most patients would consider the cholinergic drugs, donepezil, galantamine and << rivastigmine >>, to be the first line pharmacotherapy for mild to moderate Alzheimer's disease.The drugs have slightly different pharmacological properties, but they all work by inhibiting the breakdown of acetylcholine, an important neurotransmitter associated with memory, by blocking the enzyme [[ acetylcholinesterase ]].


BACKGROUND: Since the introduction of the first cholinesterase inhibitor (ChEI) in 1997, most clinicians and probably most patients would consider the cholinergic drugs, donepezil, galantamine and rivastigmine, to be the first line pharmacotherapy for mild to moderate Alzheimer's disease.The drugs have slightly different pharmacological properties, but they all work by inhibiting the breakdown of << acetylcholine >>, an important neurotransmitter associated with memory, by blocking the enzyme [[ acetylcholinesterase ]].


Mitiglinide (<< KAD-1229 >>), a new anti-diabetic drug, is thought to stimulate [[ insulin ]] secretion by closing the ATP-sensitive K+ (K(ATP)) channels in pancreatic beta-cells.


<< Mitiglinide >> (KAD-1229), a new anti-diabetic drug, is thought to stimulate [[ insulin ]] secretion by closing the ATP-sensitive K+ (K(ATP)) channels in pancreatic beta-cells.


Mitiglinide (<< KAD-1229 >>), a new anti-diabetic drug, is thought to stimulate insulin secretion by closing the [[ ATP-sensitive K+ (K(ATP)) channels ]] in pancreatic beta-cells.


<< Mitiglinide >> (KAD-1229), a new anti-diabetic drug, is thought to stimulate insulin secretion by closing the [[ ATP-sensitive K+ (K(ATP)) channels ]] in pancreatic beta-cells.


Patch-clamp analysis using inside-out recording configuration showed that << mitiglinide >> inhibits the [[ Kir6.2 ]]/SUR1 channel currents in a dose-dependent manner (IC50 value, 100 nM) but does not significantly inhibit either Kir6.2/SUR2A or Kir6.2/SUR2B channel currents even at high doses (more than 10 microM).


Patch-clamp analysis using inside-out recording configuration showed that << mitiglinide >> inhibits the Kir6.2/[[ SUR1 ]] channel currents in a dose-dependent manner (IC50 value, 100 nM) but does not significantly inhibit either Kir6.2/SUR2A or Kir6.2/SUR2B channel currents even at high doses (more than 10 microM).


<< Nateglinide >> inhibits [[ Kir6.2 ]]/SUR1 and Kir6.2/SUR2B channels at 100 nM, and inhibits Kir6.2/SUR2A channels at high concentrations (1 microM).


<< Nateglinide >> inhibits Kir6.2/[[ SUR1 ]] and Kir6.2/SUR2B channels at 100 nM, and inhibits Kir6.2/SUR2A channels at high concentrations (1 microM).


<< Nateglinide >> inhibits Kir6.2/SUR1 and [[ Kir6.2 ]]/SUR2B channels at 100 nM, and inhibits Kir6.2/SUR2A channels at high concentrations (1 microM).


<< Nateglinide >> inhibits Kir6.2/SUR1 and Kir6.2/[[ SUR2B ]] channels at 100 nM, and inhibits Kir6.2/SUR2A channels at high concentrations (1 microM).


<< Nateglinide >> inhibits Kir6.2/SUR1 and Kir6.2/SUR2B channels at 100 nM, and inhibits [[ Kir6.2 ]]/SUR2A channels at high concentrations (1 microM).


<< Nateglinide >> inhibits Kir6.2/SUR1 and Kir6.2/SUR2B channels at 100 nM, and inhibits Kir6.2/[[ SUR2A ]] channels at high concentrations (1 microM).


These results indicate that, similar to the sulfonylureas, mitiglinide is highly specific to the Kir6.2/SUR1 complex, i.e., the pancreatic beta-cell << K(ATP) channel >>, and suggest that [[ mitiglinide ]] may be a clinically useful anti-diabetic drug.


Although generally highly specific for angiotensin II type 1 receptors, some ARBs, particularly << telmisartan >>, are partial agonists at [[ peroxisome proliferator-activated receptor-γ ]].


Although generally highly specific for << angiotensin II type 1 receptors >>, some ARBs, particularly [[ telmisartan ]], are partial agonists at peroxisome proliferator-activated receptor-γ.


Direct-acting << CB1 >> agonists, including [[ Δ(9)-tetrahydrocannabinol ]], WIN 55,212 [R-(1)-[2,3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4-benzoxazinyl]-(1-naphthalenyl)methanone mesylate], AM2389 [9β-hydroxy-3-(1-hexyl-cyclobut-1-yl)-hexahydrocannabinol], and AM4054 [9β-(hydroxymethyl)-3-(1-adamantyl)-hexahydrocannabinol], produced dose-dependent increases in diuresis and decreases in colonic temperature, with slightly lower ED(50) values for diuresis than for hypothermia.


Direct-acting << CB1 >> agonists, including Δ(9)-tetrahydrocannabinol, [[ WIN 55,212 ]] [R-(1)-[2,3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4-benzoxazinyl]-(1-naphthalenyl)methanone mesylate], AM2389 [9β-hydroxy-3-(1-hexyl-cyclobut-1-yl)-hexahydrocannabinol], and AM4054 [9β-(hydroxymethyl)-3-(1-adamantyl)-hexahydrocannabinol], produced dose-dependent increases in diuresis and decreases in colonic temperature, with slightly lower ED(50) values for diuresis than for hypothermia.


Direct-acting << CB1 >> agonists, including Δ(9)-tetrahydrocannabinol, WIN 55,212 [[[ R-(1)-[2,3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4-benzoxazinyl]-(1-naphthalenyl)methanone mesylate ]]], AM2389 [9β-hydroxy-3-(1-hexyl-cyclobut-1-yl)-hexahydrocannabinol], and AM4054 [9β-(hydroxymethyl)-3-(1-adamantyl)-hexahydrocannabinol], produced dose-dependent increases in diuresis and decreases in colonic temperature, with slightly lower ED(50) values for diuresis than for hypothermia.


Direct-acting << CB1 >> agonists, including Δ(9)-tetrahydrocannabinol, WIN 55,212 [R-(1)-[2,3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4-benzoxazinyl]-(1-naphthalenyl)methanone mesylate], [[ AM2389 ]] [9β-hydroxy-3-(1-hexyl-cyclobut-1-yl)-hexahydrocannabinol], and AM4054 [9β-(hydroxymethyl)-3-(1-adamantyl)-hexahydrocannabinol], produced dose-dependent increases in diuresis and decreases in colonic temperature, with slightly lower ED(50) values for diuresis than for hypothermia.


Direct-acting << CB1 >> agonists, including Δ(9)-tetrahydrocannabinol, WIN 55,212 [R-(1)-[2,3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4-benzoxazinyl]-(1-naphthalenyl)methanone mesylate], AM2389 [[[ 9β-hydroxy-3-(1-hexyl-cyclobut-1-yl)-hexahydrocannabinol ]]], and AM4054 [9β-(hydroxymethyl)-3-(1-adamantyl)-hexahydrocannabinol], produced dose-dependent increases in diuresis and decreases in colonic temperature, with slightly lower ED(50) values for diuresis than for hypothermia.


Direct-acting << CB1 >> agonists, including Δ(9)-tetrahydrocannabinol, WIN 55,212 [R-(1)-[2,3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4-benzoxazinyl]-(1-naphthalenyl)methanone mesylate], AM2389 [9β-hydroxy-3-(1-hexyl-cyclobut-1-yl)-hexahydrocannabinol], and [[ AM4054 ]] [9β-(hydroxymethyl)-3-(1-adamantyl)-hexahydrocannabinol], produced dose-dependent increases in diuresis and decreases in colonic temperature, with slightly lower ED(50) values for diuresis than for hypothermia.


Direct-acting << CB1 >> agonists, including Δ(9)-tetrahydrocannabinol, WIN 55,212 [R-(1)-[2,3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4-benzoxazinyl]-(1-naphthalenyl)methanone mesylate], AM2389 [9β-hydroxy-3-(1-hexyl-cyclobut-1-yl)-hexahydrocannabinol], and AM4054 [[[ 9β-(hydroxymethyl)-3-(1-adamantyl)-hexahydrocannabinol ]]], produced dose-dependent increases in diuresis and decreases in colonic temperature, with slightly lower ED(50) values for diuresis than for hypothermia.


Methanandamide (10.0 mg/kg) had lesser effect than other CB agonists, and the << CB2 >> agonist [[ AM1241 ]] [1-(methylpiperidin-2-ylmethyl)-3-(2-iodo-5-nitrobenzoyl)indole], the anandamide transport inhibitor AM404, and the CB antagonist rimonabant did not have diuretic effects.


Methanandamide (10.0 mg/kg) had lesser effect than other CB agonists, and the << CB2 >> agonist AM1241 [[[ 1-(methylpiperidin-2-ylmethyl)-3-(2-iodo-5-nitrobenzoyl)indole ]]], the anandamide transport inhibitor AM404, and the CB antagonist rimonabant did not have diuretic effects.


Methanandamide (10.0 mg/kg) had lesser effect than other CB agonists, and the << CB2 >> agonist AM1241 [1-(methylpiperidin-2-ylmethyl)-3-(2-iodo-5-nitrobenzoyl)indole], the anandamide transport inhibitor [[ AM404 ]], and the CB antagonist rimonabant did not have diuretic effects.


In further studies, the diuretic effects of the << CB1 >> agonist [[ AM4054 ]] were similar in male and female rats, displayed a relatively rapid onset to action, and were dose-dependently antagonized by 30 minutes pretreatment with rimonabant, but not by the vanilloid receptor type I antagonist capsazepine, nor were the effects of WIN 55,212 antagonized by the CB2 antagonist AM630 [(6-iodo-2-methyl-1-[2-(4-morpholinyl)ethyl]-1H-indol-3-yl](4-methoxyphenyl) methanone)].


In further studies, the diuretic effects of the CB1 agonist AM4054 were similar in male and female rats, displayed a relatively rapid onset to action, and were dose-dependently antagonized by 30 minutes pretreatment with rimonabant, but not by the vanilloid receptor type I antagonist capsazepine, nor were the effects of << WIN 55,212 >> antagonized by the [[ CB2 ]] antagonist AM630 [(6-iodo-2-methyl-1-[2-(4-morpholinyl)ethyl]-1H-indol-3-yl](4-methoxyphenyl) methanone)].


In further studies, the diuretic effects of the << CB1 >> agonist AM4054 were similar in male and female rats, displayed a relatively rapid onset to action, and were dose-dependently antagonized by 30 minutes pretreatment with [[ rimonabant ]], but not by the vanilloid receptor type I antagonist capsazepine, nor were the effects of WIN 55,212 antagonized by the CB2 antagonist AM630 [(6-iodo-2-methyl-1-[2-(4-morpholinyl)ethyl]-1H-indol-3-yl](4-methoxyphenyl) methanone)].


In further studies, the diuretic effects of the CB1 agonist AM4054 were similar in male and female rats, displayed a relatively rapid onset to action, and were dose-dependently antagonized by 30 minutes pretreatment with rimonabant, but not by the << vanilloid receptor type I >> antagonist [[ capsazepine ]], nor were the effects of WIN 55,212 antagonized by the CB2 antagonist AM630 [(6-iodo-2-methyl-1-[2-(4-morpholinyl)ethyl]-1H-indol-3-yl](4-methoxyphenyl) methanone)].


In further studies, the diuretic effects of the CB1 agonist AM4054 were similar in male and female rats, displayed a relatively rapid onset to action, and were dose-dependently antagonized by 30 minutes pretreatment with rimonabant, but not by the vanilloid receptor type I antagonist capsazepine, nor were the effects of WIN 55,212 antagonized by the << CB2 >> antagonist [[ AM630 ]] [(6-iodo-2-methyl-1-[2-(4-morpholinyl)ethyl]-1H-indol-3-yl](4-methoxyphenyl) methanone)].


In further studies, the diuretic effects of the CB1 agonist AM4054 were similar in male and female rats, displayed a relatively rapid onset to action, and were dose-dependently antagonized by 30 minutes pretreatment with rimonabant, but not by the vanilloid receptor type I antagonist capsazepine, nor were the effects of WIN 55,212 antagonized by the << CB2 >> antagonist AM630 [[[ (6-iodo-2-methyl-1-[2-(4-morpholinyl)ethyl]-1H-indol-3-yl](4-methoxyphenyl) methanone) ]]].


<< N-[2-(cyclohexyloxyl)-4-nitrophenyl]-methanesulfonamide >> (NS-398), a selective [[ cyclooxygenase-2 ]] inhibitor, also inhibited cell proliferation, whereas it did not cause apoptosis.


N-[2-(cyclohexyloxyl)-4-nitrophenyl]-methanesulfonamide (<< NS-398 >>), a selective [[ cyclooxygenase-2 ]] inhibitor, also inhibited cell proliferation, whereas it did not cause apoptosis.


Mutation of arginine 228 to << lysine >> enhances the [[ glucosyltransferase ]] activity of bovine beta-1,4-galactosyltransferase I.


Beta-1,4-galactosyltransferase I (beta4Gal-T1) normally transfers Gal from UDP-Gal to GlcNAc in the presence of Mn(2+) ion (Gal-T activity) and also transfers Glc from << UDP-Glc >> to GlcNAc ([[ Glc-T ]] activity), albeit at only 0.3% efficiency.


<< Beta-1,4-galactosyltransferase I >> (beta4Gal-T1) normally transfers Gal from [[ UDP-Gal ]] to GlcNAc in the presence of Mn(2+) ion (Gal-T activity) and also transfers Glc from UDP-Glc to GlcNAc (Glc-T activity), albeit at only 0.3% efficiency.


Beta-1,4-galactosyltransferase I (beta4Gal-T1) normally transfers Gal from << UDP-Gal >> to GlcNAc in the presence of Mn(2+) ion ([[ Gal-T ]] activity) and also transfers Glc from UDP-Glc to GlcNAc (Glc-T activity), albeit at only 0.3% efficiency.


Beta-1,4-galactosyltransferase I (<< beta4Gal-T1 >>) normally transfers Gal from [[ UDP-Gal ]] to GlcNAc in the presence of Mn(2+) ion (Gal-T activity) and also transfers Glc from UDP-Glc to GlcNAc (Glc-T activity), albeit at only 0.3% efficiency.


Discovery of novel << 2-hydroxydiarylamide >> derivatives as [[ TMPRSS4 ]] inhibitors.


In this study, a novel series of << 2-hydroxydiarylamide >> derivatives were synthesized and evaluated for inhibiting [[ TMPRSS4 ]] serine protease activity and suppressing cancer cell invasion.


In this study, a novel series of << 2-hydroxydiarylamide >> derivatives were synthesized and evaluated for inhibiting TMPRSS4 [[ serine protease ]] activity and suppressing cancer cell invasion.


The selective << betaAR >> agonist [[ isoproterenol ]] caused an enhancement of hippocampal CA3 network activity, as measured by an increase in frequency of spontaneous burst discharges recorded in the CA3 region.


The selective << beta1AR >> antagonists atenolol and metoprolol blocked [[ isoproterenol ]]-induced enhancement, with apparent K(b) values of 85 +/- 36 and 3.9 +/- 1.7 nM, respectively.


The selective << beta1AR >> antagonists [[ atenolol ]] and metoprolol blocked isoproterenol-induced enhancement, with apparent K(b) values of 85 +/- 36 and 3.9 +/- 1.7 nM, respectively.


The selective << beta1AR >> antagonists atenolol and [[ metoprolol ]] blocked isoproterenol-induced enhancement, with apparent K(b) values of 85 +/- 36 and 3.9 +/- 1.7 nM, respectively.


In contrast, the selective << beta2AR >> antagonists ICI-118,551 and butoxamine inhibited [[ isoproterenol ]]-mediated enhancement with apparent low affinities (K(b) of 222 +/- 61 and 9268 +/- 512 nM, respectively).


In contrast, the selective << beta2AR >> antagonists ICI-118,551 and [[ butoxamine ]] inhibited isoproterenol-mediated enhancement with apparent low affinities (K(b) of 222 +/- 61 and 9268 +/- 512 nM, respectively).


In contrast, the selective << beta2AR >> antagonists [[ ICI-118,551 ]] and butoxamine inhibited isoproterenol-mediated enhancement with apparent low affinities (K(b) of 222 +/- 61 and 9268 +/- 512 nM, respectively).


Together, this pharmacological profile of subtype-selective betaAR antagonists indicates that in this model, << beta1AR >> activation is responsible for the enhanced hippocampal CA3 network activity initiated by [[ isoproterenol ]].


<< P2Y(2) receptor >> agonist [[ INS37217 ]] enhances functional recovery after detachment caused by subretinal injection in normal and rds mice.


Selective antagonism of << GluR5 >> kainate-receptor-mediated synaptic currents by [[ topiramate ]] in rat basolateral amygdala neurons.


Selective antagonism of GluR5 << kainate-receptor >>-mediated synaptic currents by [[ topiramate ]] in rat basolateral amygdala neurons.


In whole-cell voltage-clamp recordings from principal neurons of the rat basolateral amygdala, << topiramate >> at low concentrations (IC50, approximately 0.5 microm) selectively inhibited pharmacologically isolated excitatory synaptic currents mediated by [[ kainate receptors ]] containing the GluR5 subunit.


In whole-cell voltage-clamp recordings from principal neurons of the rat basolateral amygdala, << topiramate >> at low concentrations (IC50, approximately 0.5 microm) selectively inhibited pharmacologically isolated excitatory synaptic currents mediated by kainate receptors containing the [[ GluR5 ]] subunit.


<< Topiramate >> also partially depressed predominantly [[ AMPA-receptor ]]-mediated EPSCs, but with lower efficacy.


Inhibition of << GluR5 >> kainate receptors could represent a key mechanism underlying the anticonvulsant activity of [[ topiramate ]].


Inhibition of GluR5 << kainate receptors >> could represent a key mechanism underlying the anticonvulsant activity of [[ topiramate ]].


Density functional theory calculations using the hybrid functional B3LYP have been performed to study the << methyl >> transfer step in [[ glycine N-methyltransferase ]] (GNMT).


Density functional theory calculations using the hybrid functional B3LYP have been performed to study the << methyl >> transfer step in glycine N-methyltransferase ([[ GNMT ]]).


The starting point for the calculations is the recent X-ray crystal structure of << GNMT >> complexed with [[ SAM ]] and acetate.


<< Dasatinib >> (BMS-354825) inhibits [[ KIT ]]D816V, an imatinib-resistant activating mutation that triggers neoplastic growth in most patients with systemic mastocytosis.


<< Dasatinib >> (BMS-354825) inhibits KIT[[ D816V ]], an imatinib-resistant activating mutation that triggers neoplastic growth in most patients with systemic mastocytosis.


Dasatinib (<< BMS-354825 >>) inhibits KIT[[ D816V ]], an imatinib-resistant activating mutation that triggers neoplastic growth in most patients with systemic mastocytosis.


<< Dasatinib >> (BMS-354825) is a novel orally bioavailable [[ SRC ]]/ABL inhibitor that has activity against multiple imatinib-resistant BCR-ABL isoforms in vitro that is presently showing considerable promise in early-phase clinical trials of chronic myeloid leukemia (CML).


<< Dasatinib >> (BMS-354825) is a novel orally bioavailable SRC/[[ ABL ]] inhibitor that has activity against multiple imatinib-resistant BCR-ABL isoforms in vitro that is presently showing considerable promise in early-phase clinical trials of chronic myeloid leukemia (CML).


Dasatinib (<< BMS-354825 >>) is a novel orally bioavailable [[ SRC ]]/ABL inhibitor that has activity against multiple imatinib-resistant BCR-ABL isoforms in vitro that is presently showing considerable promise in early-phase clinical trials of chronic myeloid leukemia (CML).


Dasatinib (<< BMS-354825 >>) is a novel orally bioavailable SRC/[[ ABL ]] inhibitor that has activity against multiple imatinib-resistant BCR-ABL isoforms in vitro that is presently showing considerable promise in early-phase clinical trials of chronic myeloid leukemia (CML).


In this study, we demonstrate significant inhibitory activity of << dasatinib >> against both wild-type [[ KIT ]] and the KITD816V mutation in the nanomolar range in in vitro and cell-based kinase assays.


In this study, we demonstrate significant inhibitory activity of << dasatinib >> against both wild-type KIT and the [[ KIT ]]D816V mutation in the nanomolar range in in vitro and cell-based kinase assays.


In this study, we demonstrate significant inhibitory activity of << dasatinib >> against both wild-type KIT and the KIT[[ D816V ]] mutation in the nanomolar range in in vitro and cell-based kinase assays.


Additionally, << dasatinib >> leads to growth inhibition of a [[ KIT ]]D816V-harboring human masto-cytosis cell line.


Additionally, << dasatinib >> leads to growth inhibition of a KIT[[ D816V ]]-harboring human masto-cytosis cell line.


Dopamine D(2) receptor-induced << COX-2 >>-mediated production of [[ prostaglandin E(2) ]] in D(2)-transfected Chinese hamster ovary cells without simultaneous administration of a Ca(2+)-mobilizing agent.


The effect was counteracted by the << D(2) >> antagonist [[ eticlopride ]], pertussis toxin, the inhibitor of intracellular Ca(2+) release TMB-8, incubation in Ca(2+)-free experimental medium, and PKC desensitization obtained by chronic pretreatment with the phorbol ester TPA.


It was also antagonized by the non-specific << cyclooxygenase >> (COX) inhibitor, [[ indomethacin ]], and by the selective COX-2 inhibitor, NS-398, but not by the specific COX-1 inhibitor, valeryl salicylate.


It was also antagonized by the non-specific cyclooxygenase (<< COX >>) inhibitor, [[ indomethacin ]], and by the selective COX-2 inhibitor, NS-398, but not by the specific COX-1 inhibitor, valeryl salicylate.


It was also antagonized by the non-specific cyclooxygenase (COX) inhibitor, indomethacin, and by the selective << COX-2 >> inhibitor, [[ NS-398 ]], but not by the specific COX-1 inhibitor, valeryl salicylate.


It was also antagonized by the non-specific cyclooxygenase (COX) inhibitor, indomethacin, and by the selective COX-2 inhibitor, NS-398, but not by the specific << COX-1 >> inhibitor, [[ valeryl salicylate ]].


Both the non-specific << phospholipase A(2) >> inhibitor, [[ quinacrine ]], and an inhibitor of cPLA(2) and iPLA(2), AACOF3, counteracted the effect; in contrast, a selective iPLA(2) inhibitor, BEL, and a selective sPLA(2) inhibitor, TAPC, were ineffective.


The results reinforce previous assumptions that << dopamine >> may interact with eicosanoid metabolism by means of [[ D(2) receptor ]] activation, and implicate an involvement of cPLA(2) and COX-2 in this effect.


A high throughput assay for the glucuronidation of << 7-hydroxy-4-trifluoromethylcoumarin >> by recombinant [[ human UDP-glucuronosyltransferases ]] and liver microsomes.


2.  We have developed a convenient quantitative multi-well plate assay to measure the glucuronidation rate of << 7-hydroxy-4-trifluoromethylcoumarin >> (HFC) for several [[ UGTs ]].


2.  We have developed a convenient quantitative multi-well plate assay to measure the glucuronidation rate of 7-hydroxy-4-trifluoromethylcoumarin (<< HFC >>) for several [[ UGTs ]].


3.  We have used this method to screen 11 recombinant << human UGTs >> for [[ HFC ]] glucuronidation activity and studied the reaction kinetics with the most active enzymes.


4.  At a substrate concentration of 20 µM, the most active << HFC >> glucuronidation catalysts were [[ UGT1A10 ]] followed by UGT1A6 >UGT1A7 >UGT2A1, whereas at 300 µM UGT1A6 was about 10 times better catalyst than the other recombinant UGTs.


4.  At a substrate concentration of 20 µM, the most active << HFC >> glucuronidation catalysts were UGT1A10 followed by [[ UGT1A6 ]] >UGT1A7 >UGT2A1, whereas at 300 µM UGT1A6 was about 10 times better catalyst than the other recombinant UGTs.


4.  At a substrate concentration of 20 µM, the most active << HFC >> glucuronidation catalysts were UGT1A10 followed by UGT1A6 >[[ UGT1A7 ]] >UGT2A1, whereas at 300 µM UGT1A6 was about 10 times better catalyst than the other recombinant UGTs.


4.  At a substrate concentration of 20 µM, the most active << HFC >> glucuronidation catalysts were UGT1A10 followed by UGT1A6 >UGT1A7 >[[ UGT2A1 ]], whereas at 300 µM UGT1A6 was about 10 times better catalyst than the other recombinant UGTs.


4.  At a substrate concentration of 20 µM, the most active << HFC >> glucuronidation catalysts were UGT1A10 followed by UGT1A6 >UGT1A7 >UGT2A1, whereas at 300 µM [[ UGT1A6 ]] was about 10 times better catalyst than the other recombinant UGTs.


4.  At a substrate concentration of 20 µM, the most active << HFC >> glucuronidation catalysts were UGT1A10 followed by UGT1A6 >UGT1A7 >UGT2A1, whereas at 300 µM UGT1A6 was about 10 times better catalyst than the other recombinant [[ UGTs ]].


UGT1A6 exhibited a significantly higher Vmax and Km values toward both << HFC >> and UDP-glucuronic acid than the other [[ UGTs ]].


<< UGT1A6 >> exhibited a significantly higher Vmax and Km values toward both [[ HFC ]] and UDP-glucuronic acid than the other UGTs.


UGT1A6 exhibited a significantly higher Vmax and Km values toward both HFC and << UDP >>-glucuronic acid than the other [[ UGTs ]].


<< UGT1A6 >> exhibited a significantly higher Vmax and Km values toward both HFC and [[ UDP ]]-glucuronic acid than the other UGTs.


UGT1A6 exhibited a significantly higher Vmax and Km values toward both HFC and UDP-<< glucuronic acid >> than the other [[ UGTs ]].


<< UGT1A6 >> exhibited a significantly higher Vmax and Km values toward both HFC and UDP-[[ glucuronic acid ]] than the other UGTs.


This inhibition was blocked when mice were pretreated with the selective << H3R >> agonist [[ R-(alpha)-methyl-histamine ]] (10 mg/kg).


The 5-HT(1/2/5/7)-receptor antagonist methysergide and the 5-HT(2A/2B/2C)-receptor antagonist LY 53857 enhanced clomipramine-induced hyperglycemia, while the << 5-HT(1A/1B)-receptor >> antagonist [[ (-)-propranolol ]] and the 5-HT(3/4)-receptor antagonist tropisetron did not affect it.


The 5-HT(1/2/5/7)-receptor antagonist methysergide and the 5-HT(2A/2B/2C)-receptor antagonist LY 53857 enhanced clomipramine-induced hyperglycemia, while the 5-HT(1A/1B)-receptor antagonist (-)-propranolol and the << 5-HT(3/4)-receptor >> antagonist [[ tropisetron ]] did not affect it.


The 5-HT(1/2/5/7)-receptor antagonist methysergide and the << 5-HT(2A/2B/2C)-receptor >> antagonist [[ LY 53857 ]] enhanced clomipramine-induced hyperglycemia, while the 5-HT(1A/1B)-receptor antagonist (-)-propranolol and the 5-HT(3/4)-receptor antagonist tropisetron did not affect it.


The << 5-HT(2B/2C)-receptor >> antagonist [[ SB 206553 ]] facilitated hyperglycemia induced by clomipramine, although the 5-HT(2A)-receptor antagonist ketanserin was without effect.


The 5-HT(2B/2C)-receptor antagonist SB 206553 facilitated hyperglycemia induced by clomipramine, although the << 5-HT(2A) >>-receptor antagonist [[ ketanserin ]] was without effect.


These results suggest that << clomipramine >> induces hyperglycemia in mice by blocking the [[ 5-HT(2B ) ]]and/or 5-HT(2C) receptors, which results in facilitation of adrenaline release.


These results suggest that << clomipramine >> induces hyperglycemia in mice by blocking the 5-HT(2B )and/or [[ 5-HT(2C) ]] receptors, which results in facilitation of adrenaline release.


<< Phosphatidylserine >> (PtdSer) is made in mammalian cells by two [[ PtdSer synthases ]], PSS1 and PSS2.


<< Phosphatidylserine >> (PtdSer) is made in mammalian cells by two PtdSer synthases, [[ PSS1 ]] and PSS2.


<< Phosphatidylserine >> (PtdSer) is made in mammalian cells by two PtdSer synthases, PSS1 and [[ PSS2 ]].


Moreover, a normal level of expression of << PSS1 >> and/or PSS2 is not required for generating the pool of [[ PtdSer ]] externalized during apoptosis.


Moreover, a normal level of expression of PSS1 and/or << PSS2 >> is not required for generating the pool of [[ PtdSer ]] externalized during apoptosis.


<< PKC >> isoforms did show different sensitivity and selectivity for down-regulation by [[ I3A ]] and phorbol 12-myristate 13-acetate (PMA) in WEHI-231, HOP-92, and Colo-205 cells.


<< PKC >> isoforms did show different sensitivity and selectivity for down-regulation by I3A and [[ phorbol 12-myristate 13-acetate ]] (PMA) in WEHI-231, HOP-92, and Colo-205 cells.


<< PKC >> isoforms did show different sensitivity and selectivity for down-regulation by I3A and phorbol 12-myristate 13-acetate ([[ PMA ]]) in WEHI-231, HOP-92, and Colo-205 cells.


<< I3A >> induced a higher level of secretion of the inflammatory cytokine [[ interleukin 6 ]] compared with PMA in the WEHI-231 cells and displayed a marked biphasic dose-response curve for the induction.


<< I3A >> induced a higher level of secretion of the inflammatory [[ cytokine ]] interleukin 6 compared with PMA in the WEHI-231 cells and displayed a marked biphasic dose-response curve for the induction.


I3A induced a higher level of secretion of the inflammatory cytokine << interleukin 6 >> compared with [[ PMA ]] in the WEHI-231 cells and displayed a marked biphasic dose-response curve for the induction.


I3A induced a higher level of secretion of the inflammatory << cytokine >> interleukin 6 compared with [[ PMA ]] in the WEHI-231 cells and displayed a marked biphasic dose-response curve for the induction.


The in vitro kinase activity of << PKC-alpha >> induced by [[ I3A ]] was lower than that induced by PMA.


The in vitro kinase activity of << PKC-alpha >> induced by I3A was lower than that induced by [[ PMA ]].


<< Type I deiodinase >>, liver fatty-acid binding protein and cytochrome P450 (CYP) 3A37 mRNA levels were significantly induced by [[ TCPP ]], while TDCPP induced CYP3A37 and CYP2H1.


Type I deiodinase, << liver fatty-acid binding protein >> and cytochrome P450 (CYP) 3A37 mRNA levels were significantly induced by [[ TCPP ]], while TDCPP induced CYP3A37 and CYP2H1.


Type I deiodinase, liver fatty-acid binding protein and << cytochrome P450 (CYP) 3A37 >> mRNA levels were significantly induced by [[ TCPP ]], while TDCPP induced CYP3A37 and CYP2H1.


Type I deiodinase, liver fatty-acid binding protein and cytochrome P450 (CYP) 3A37 mRNA levels were significantly induced by TCPP, while << TDCPP >> induced [[ CYP3A37 ]] and CYP2H1.


Type I deiodinase, liver fatty-acid binding protein and cytochrome P450 (CYP) 3A37 mRNA levels were significantly induced by TCPP, while << TDCPP >> induced CYP3A37 and [[ CYP2H1 ]].


The results suggested that both the << EtOAc >> extract and berberine were able to activate [[ PPARα/β/γ ]], and Rhizoma Coptis contains potential natural agonists of PPARs besides berberine.


The results suggested that both the EtOAc extract and << berberine >> were able to activate [[ PPARα/β/γ ]], and Rhizoma Coptis contains potential natural agonists of PPARs besides berberine.


The results suggested that both the EtOAc extract and berberine were able to activate << PPARα/β/γ >>, and Rhizoma Coptis contains potential natural agonists of PPARs besides [[ berberine ]].


The results suggested that both the EtOAc extract and berberine were able to activate PPARα/β/γ, and Rhizoma Coptis contains potential natural agonists of << PPARs >> besides [[ berberine ]].


This hypothesis was tested by investigating whether, in subjects with essential hypertension, the natriuretic response to specific << renin >>-angiotensin-aldosterone system (RAAS) blockade by renin-inhibitor [[ remikiren ]] could be predicted from pretreatment renal vascular tone.


This hypothesis was tested by investigating whether, in subjects with essential hypertension, the natriuretic response to specific renin-<< angiotensin >>-aldosterone system (RAAS) blockade by renin-inhibitor [[ remikiren ]] could be predicted from pretreatment renal vascular tone.


This hypothesis was tested by investigating whether, in subjects with essential hypertension, the natriuretic response to specific renin-angiotensin-aldosterone system (RAAS) blockade by << renin >>-inhibitor [[ remikiren ]] could be predicted from pretreatment renal vascular tone.


TREK-1 currents are insensitive to pharmacological agents that block << TWIK-1 >> activity such as [[ quinine ]] and quinidine.


TREK-1 currents are insensitive to pharmacological agents that block << TWIK-1 >> activity such as quinine and [[ quinidine ]].


<< CGP 12177A >> mediates cardiostimulation by activation of the 'putative' [[ beta(4)-adrenoceptor ]]; however, it has recently been reported that disruption of the beta(1)-adrenoceptor gene abolishes this effect.


<< CGP 12177A >> mediates cardiostimulation by activation of the 'putative' beta(4)-adrenoceptor; however, it has recently been reported that disruption of the [[ beta(1)-adrenoceptor ]] gene abolishes this effect.


<< CGP 12177A >> but not isoprenaline initiated arrhythmias at lower concentrations following [[ beta(1)-adrenoceptor ]] overexpression.


<< (125)I-Cyanopindolol >> saturation binding in Adv.beta(1) myocytes demonstrated approximately 18-fold increase in [[ beta(1)-adrenoceptors ]].


(3)H-CGP 12177A saturation binding, in the presence of << propranolol >>, increased approximately 5-fold following overexpression of [[ beta(1)-adrenoceptors ]].


<< (3)H-CGP 12177A >> saturation binding, in the presence of propranolol, increased approximately 5-fold following overexpression of [[ beta(1)-adrenoceptors ]].


In contrast, in the presence of << Ca >> UFH accelerated the inhibition of [[ factor Xa ]] by antithrombin 10-fold more efficiently than comparable concentrations of the high affinity fractions of enoxaparin and fragmin.


In contrast, in the presence of << Ca >> UFH accelerated the inhibition of factor Xa by [[ antithrombin ]] 10-fold more efficiently than comparable concentrations of the high affinity fractions of enoxaparin and fragmin.


INTRODUCTION: The principal aim of this study was to assess the efficacy of << quinidine >> in suppressing [[ IKr ]] in vitro and in modulating the rate dependence of the QT interval in the "SQT1" form of the short QT syndrome.


CONCLUSION: Oral << quinidine >> is effective in suppressing the gain of function in [[ IKr ]] responsible for some cases of short QT syndrome with a mutation in HERG and thus restoring normal rate dependence of the QT interval and rendering ventricular tachycardia/ventricular fibrillation noninducible.


The IC50-values obtained for the inhibition of lipopolysaccharide (LPS)-induced release of prostaglandin E2 (PGE2) reflecting << cyclooxygenase (COX)-2 >>-mediated [[ PGE2 ]] release were 47 microg/ml and 0.6 microg/ml, for the Salix extract 1520L and rofecoxib-like research compound L745337, respectively.


Our results indicate that Salix extract 1520L inhibits << COX-2 >>-mediated [[ PGE2 ]] release through compounds other than salicin or salicylate.


<< Follicle-stimulating hormone >> (FSH), a dimeric glycoprotein synthesized in the anterior pituitary gland, is important for the production of sex [[ steroids ]] and gametes.


Follicle-stimulating hormone (<< FSH >>), a dimeric glycoprotein synthesized in the anterior pituitary gland, is important for the production of sex [[ steroids ]] and gametes.


Humans with << FSH beta >> gene mutations tend to have a more severe phenotype than those with FSHR gene mutations, although infertility and varying degrees of impaired sex [[ steroid ]] production occur in both types of mutations.


OBJECTIVES: The aim of the current study was to assess the activity of << rolipram >>, a nonsubtype-selective [[ PDE4 ]] inhibitor, in several animal models predictive of antipsychotic-like efficacy and side-effect liability and to use PDE4B wild-type and knockout mice to begin to understand the subtypes involved in the activity of rolipram.


These results suggest that PDE4B mediates the antipsychotic effects of rolipram in CAR and that the << PDE4B >>-regulated [[ cyclic adenosine monophosphate ]] signaling pathway may play a role in the pathophysiology and pharmacotherapy of psychosis.


<< Cat-1 >>, the transporter for the essential [[ amino acids ]], arginine and lysine, is one of the up-regulated genes.


<< Cat-1 >>, the transporter for the essential amino acids, [[ arginine ]] and lysine, is one of the up-regulated genes.


<< Cat-1 >>, the transporter for the essential amino acids, arginine and [[ lysine ]], is one of the up-regulated genes.


RESULTS: Fractionated bulb extracts and the two isolated << steroidal glycoalkaloids >> (1) and (2) induced NO production and [[ TGF-β receptor I ]] mRNA expression in fibroblast cell culture.


On the basis of data obtained in rabbits, the imidazoline receptor ligand << rilmenidine >> has been suggested to decrease blood pressure in humans by activating central [[ alpha(2A)-adrenoceptors ]].


A prerequisite for this hypothesis was the unproved assumption that rabbit and human << alpha(2A)-adrenoceptors >> are equally activated by [[ rilmenidine ]].


Human atrial appendages and rabbit pulmonary arteries were used to determine the potencies of alpha(2)-adrenoceptor agonists in inhibiting the electrically (2 Hz) evoked [(3)H]norepinephrine release and of antagonists in counteracting the << alpha(2)-adrenoceptor >>-mediated inhibition induced by [[ moxonidine ]].


In the rabbit pulmonary artery, << rilmenidine >> and oxymetazoline are potent full agonists, whereas in the human atrial appendages they are antagonists at the [[ alpha(2)-autoreceptors ]], sharing this property with rauwolscine, phentolamine, and idazoxan.


In the rabbit pulmonary artery, rilmenidine and << oxymetazoline >> are potent full agonists, whereas in the human atrial appendages they are antagonists at the [[ alpha(2)-autoreceptors ]], sharing this property with rauwolscine, phentolamine, and idazoxan.


In the rabbit pulmonary artery, rilmenidine and oxymetazoline are potent full agonists, whereas in the human atrial appendages they are antagonists at the << alpha(2)-autoreceptors >>, sharing this property with [[ rauwolscine ]], phentolamine, and idazoxan.


In the rabbit pulmonary artery, rilmenidine and oxymetazoline are potent full agonists, whereas in the human atrial appendages they are antagonists at the << alpha(2)-autoreceptors >>, sharing this property with rauwolscine, [[ phentolamine ]], and idazoxan.


In the rabbit pulmonary artery, rilmenidine and oxymetazoline are potent full agonists, whereas in the human atrial appendages they are antagonists at the << alpha(2)-autoreceptors >>, sharing this property with rauwolscine, phentolamine, and [[ idazoxan ]].


The sympathetic nerves of both the human atrial appendages and rabbit pulmonary artery are endowed with << alpha(2A)-autoreceptors >>, at which, however, both rilmenidine and [[ oxymetazoline ]] exhibit different properties (antagonism and agonism, respectively).


The sympathetic nerves of both the human atrial appendages and rabbit pulmonary artery are endowed with << alpha(2A)-autoreceptors >>, at which, however, both [[ rilmenidine ]] and oxymetazoline exhibit different properties (antagonism and agonism, respectively).


The antagonistic property of << rilmenidine >> at [[ human alpha(2A)-adrenoceptors ]] indicates that in contrast to the suggestion based on rabbit data, the hypotensive property of the drug in humans is not due to activation of alpha(2A)-adrenoceptors but other, presumably I(1)-imidazoline receptors, are probably involved.


<< Cetrorelix >> completely blocked the rise of levels of the two most abundant species, 5.0 kb and 4.5 kb, of the [[ GnRH-R ]] mRNA, during both the infantile and the juvenile periods.


<< Cetrorelix >> also abolished the developmental rise of the [[ gonadotropin beta ]] subunit mRNAs during the two periods of the study.


The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosages of the nonsedating << histamine H1-receptor >> antagonists [[ terfenadine ]], astemizole, loratadine, and acrivastine are reviewed.


The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosages of the nonsedating << histamine H1-receptor >> antagonists terfenadine, [[ astemizole ]], loratadine, and acrivastine are reviewed.


The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosages of the nonsedating << histamine H1-receptor >> antagonists terfenadine, astemizole, [[ loratadine ]], and acrivastine are reviewed.


The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosages of the nonsedating << histamine H1-receptor >> antagonists terfenadine, astemizole, loratadine, and [[ acrivastine ]] are reviewed.


<< Terfenadine >> and astemizole are chemically unrelated to [[ histamine H1-receptor ]] antagonists such as diphenhydramine and chlorpheniramine.


Terfenadine and << astemizole >> are chemically unrelated to [[ histamine H1-receptor ]] antagonists such as diphenhydramine and chlorpheniramine.


Terfenadine and astemizole are chemically unrelated to << histamine H1-receptor >> antagonists such as [[ diphenhydramine ]] and chlorpheniramine.


Terfenadine and astemizole are chemically unrelated to << histamine H1-receptor >> antagonists such as diphenhydramine and [[ chlorpheniramine ]].


Anti-inflammatory effect of << prunetin >> via the suppression of [[ NF-κB ]] pathway.


Promoter assay revealed that << prunetin >> inhibits LPS-induced nitric oxide and prostaglandin E2 production through the suppression of [[ iNOS ]] and COX-2 at the transcriptional level.


Promoter assay revealed that << prunetin >> inhibits LPS-induced nitric oxide and prostaglandin E2 production through the suppression of iNOS and [[ COX-2 ]] at the transcriptional level.


In addition, << prunetin >> inhibits [[ NF-κB ]]-dependent inflammatory responses by modulating IκB kinase (IKK)-inhibitor κBα (IκBα)-NF-κB signaling.


Consistent with these results, << prunetin >> significantly reduced serum levels of inflammatory [[ cytokines ]] and mortality in mice challenged with lipopolysaccharide.


G6PC2: A Negative Regulator of Basal << Glucose >>-Stimulated [[ Insulin ]] Secretion.


G6pc2 deletion resulted in a leftward shift in the dose-response curve for << glucose >>-stimulated [[ insulin ]] secretion (GSIS).


These data suggest that << G6pc2 >> represents a novel, negative regulator of basal GSIS that acts by hydrolyzing [[ glucose-6-phosphate ]], thereby reducing glycolytic flux.


Using the << mTOR >> inhibitor [[ PP242, ]] we found that TGFβ-induced both early and sustained activation of TORC1 and TORC2 was necessary for deptor suppression.


<< PP242 >>-induced reversal of [[ deptor ]] suppression by TGFβ was associated with a significant inhibition of TGFβ-stimulated protein synthesis and hypertrophy.


METHODS: (+/-)-Modafinil and its R-(-)- and S-(+)-enantiomers were synthesized and tested for inhibition of << [(3)H] dopamine >> (DA) uptake and [(3)H]WIN 35428 binding in [[ human dopamine transporter ]] (DAT) wild-type and mutants with altered conformational equilibria.


METHODS: (+/-)-Modafinil and its R-(-)- and S-(+)-enantiomers were synthesized and tested for inhibition of << [(3)H] dopamine >> (DA) uptake and [(3)H]WIN 35428 binding in human dopamine transporter ([[ DAT ]]) wild-type and mutants with altered conformational equilibria.


METHODS: (+/-)-Modafinil and its R-(-)- and S-(+)-enantiomers were synthesized and tested for inhibition of [(3)H] dopamine (<< DA >>) uptake and [(3)H]WIN 35428 binding in [[ human dopamine transporter ]] (DAT) wild-type and mutants with altered conformational equilibria.


METHODS: (+/-)-Modafinil and its R-(-)- and S-(+)-enantiomers were synthesized and tested for inhibition of [(3)H] dopamine (<< DA >>) uptake and [(3)H]WIN 35428 binding in human dopamine transporter ([[ DAT ]]) wild-type and mutants with altered conformational equilibria.


RESULTS: (+/-)-, R-, and S-modafinil bind to the << DAT >> and inhibit [[ DA ]] uptake less potently than cocaine, with R-modafinil having approximately threefold higher affinity than its S-enantiomer.


Apple << polyphenols >> suppress antigen presentation of [[ ovalbumin ]] by THP-1-derived dendritic cells.


A significant decrease in << HLA-DR >> expression was observed in the AP and fractionated [[ procyanidin ]]-treated cells in the presence of ovalbumin (OVA), but no effect on CD86 expression was observed.


Furthermore, the up-regulation of << IL-12 >> and TNF-α was found in the [[ procyanidin ]] trimers-treated cells in the presence of OVA.


Furthermore, the up-regulation of IL-12 and << TNF-α >> was found in the [[ procyanidin ]] trimers-treated cells in the presence of OVA.


The acute toxicity of << organophosphorus >> (OP) compounds in mammals is due to their irreversible inhibition of [[ acetylcholinesterase ]] (AChE) in the nervous system, which leads to increased synaptic acetylcholine levels.


The acute toxicity of << organophosphorus >> (OP) compounds in mammals is due to their irreversible inhibition of acetylcholinesterase ([[ AChE ]]) in the nervous system, which leads to increased synaptic acetylcholine levels.


The acute toxicity of organophosphorus (OP) compounds in mammals is due to their irreversible inhibition of << acetylcholinesterase >> (AChE) in the nervous system, which leads to increased synaptic [[ acetylcholine ]] levels.


The acute toxicity of organophosphorus (OP) compounds in mammals is due to their irreversible inhibition of acetylcholinesterase (<< AChE >>) in the nervous system, which leads to increased synaptic [[ acetylcholine ]] levels.


In phosphotriesterase and physostigmine-treated mice, a 4- and 2-fold higher << sarin >> dose, respectively, was needed to cause a 50% inhibition of brain [[ AChE ]] activity.


The << CYP3A4 >> activity could be induced 2-fold by [[ rifampicin ]], whereas CYP2C9 activity remained equally high.


The CYP3A4 activity could be induced 2-fold by << rifampicin >>, whereas [[ CYP2C9 ]] activity remained equally high.


<< PF-04859989 >> as a template for structure-based drug design: identification of new pyrazole series of irreversible [[ KAT II ]] inhibitors with improved lipophilic efficiency.


PF-04859989 as a template for structure-based drug design: identification of new << pyrazole >> series of irreversible [[ KAT II ]] inhibitors with improved lipophilic efficiency.


The structure-based design, synthesis, and biological evaluation of a new << pyrazole >> series of irreversible [[ KAT II ]] inhibitors are described herein.


The modification of the inhibitor scaffold of 1 and 2 from a << dihydroquinolinone >> core to a tetrahydropyrazolopyridinone core led to discovery of a new series of potent [[ KAT II ]] inhibitors with excellent physicochemical properties.


The modification of the inhibitor scaffold of 1 and 2 from a dihydroquinolinone core to a << tetrahydropyrazolopyridinone >> core led to discovery of a new series of potent [[ KAT II ]] inhibitors with excellent physicochemical properties.


The capacity of << acetylcholinesterase >> inhibitors, with the exception of [[ tacrine ]] and ambenonium, to displace bound [3H]-oxotremorine-M in preference to [3H]quinuclinidyl benzilate predicts that the former compounds could act as potential agonists at muscarinic receptors.


The capacity of << acetylcholinesterase >> inhibitors, with the exception of tacrine and [[ ambenonium ]], to displace bound [3H]-oxotremorine-M in preference to [3H]quinuclinidyl benzilate predicts that the former compounds could act as potential agonists at muscarinic receptors.


Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> (ambenonium>neostigmine=physostigmine =tacrine>[[ pyridostigmine ]]=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.


Moreover, the rank order for potency in inhibiting acetylcholinesterase (ambenonium>neostigmine=physostigmine =tacrine><< pyridostigmine >>=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.


Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=[[ edrophonium ]]=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.


Moreover, the rank order for potency in inhibiting acetylcholinesterase (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=<< edrophonium >>=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.


Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=[[ galanthamine ]] >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.


Moreover, the rank order for potency in inhibiting acetylcholinesterase (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=<< galanthamine >> >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.


Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine >[[ desoxypeganine ]]>parathion>gramine) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.


Moreover, the rank order for potency in inhibiting acetylcholinesterase (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine ><< desoxypeganine >>>parathion>gramine) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.


Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine>[[ parathion ]]>gramine) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.


Moreover, the rank order for potency in inhibiting acetylcholinesterase (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine><< parathion >>>gramine) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.


Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion>[[ gramine ]]) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.


Moreover, the rank order for potency in inhibiting acetylcholinesterase (ambenonium>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion><< gramine >>) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.


Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> ([[ ambenonium ]]>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.


Moreover, the rank order for potency in inhibiting acetylcholinesterase (<< ambenonium >>>neostigmine=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.


Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> (ambenonium>[[ neostigmine ]]=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.


Moreover, the rank order for potency in inhibiting acetylcholinesterase (ambenonium><< neostigmine >>=physostigmine =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.


Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> (ambenonium>neostigmine=[[ physostigmine ]] =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.


Moreover, the rank order for potency in inhibiting acetylcholinesterase (ambenonium>neostigmine=<< physostigmine >> =tacrine>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.


Moreover, the rank order for potency in inhibiting << acetylcholinesterase >> (ambenonium>neostigmine=physostigmine =[[ tacrine ]]>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of acetylcholinesterase also displaced [3H]-oxotremorine-M to the greatest extent.


Moreover, the rank order for potency in inhibiting acetylcholinesterase (ambenonium>neostigmine=physostigmine =<< tacrine >>>pyridostigmine=edrophonium=galanthamine >desoxypeganine>parathion>gramine) indicated that the most effective inhibitors of [[ acetylcholinesterase ]] also displaced [3H]-oxotremorine-M to the greatest extent.


CONCLUSIONS: Total vitamin B6 is abnormally high in autism, consistent with previous reports of an impaired << pyridoxal kinase >> for the conversion of pyridoxine and pyridoxal to [[ PLP ]].


CONCLUSIONS: Total vitamin B6 is abnormally high in autism, consistent with previous reports of an impaired << pyridoxal kinase >> for the conversion of [[ pyridoxine ]] and pyridoxal to PLP.


CONCLUSIONS: Total vitamin B6 is abnormally high in autism, consistent with previous reports of an impaired << pyridoxal kinase >> for the conversion of pyridoxine and [[ pyridoxal ]] to PLP.


Synthesis, molecular modeling and evaluation of novel << N'-2-(4-benzylpiperidin-/piperazin-1-yl)acylhydrazone >> derivatives as dual inhibitors for [[ cholinesterases ]] and Aβ aggregation.


Synthesis, molecular modeling and evaluation of novel << N'-2-(4-benzylpiperidin-/piperazin-1-yl)acylhydrazone >> derivatives as dual inhibitors for cholinesterases and [[ Aβ ]] aggregation.


To develop new drugs for treatment of Alzheimer's disease, a group of << N'-2-(4-Benzylpiperidin-/piperazin-1-yl)acylhydrazones >> was designed, synthesized and tested for their ability to inhibit [[ acetylcholinesterase ]], butyrylcholinesterase and aggregation of amyloid beta peptides (1-40, 1-42 and 1-40_1-42).


To develop new drugs for treatment of Alzheimer's disease, a group of << N'-2-(4-Benzylpiperidin-/piperazin-1-yl)acylhydrazones >> was designed, synthesized and tested for their ability to inhibit acetylcholinesterase, [[ butyrylcholinesterase ]] and aggregation of amyloid beta peptides (1-40, 1-42 and 1-40_1-42).


β-Amyloid aggregation results showed that all compounds exhibited remarkable << Aβ >> fibril aggregation inhibition activity with a nearly similar potential as the reference compound [[ rifampicin ]], which makes them promising anti-Alzheimer drug candidates.


Here, translocation studies using the human androgen receptor (hAR) and the human glucocorticoid receptor (hGR) were performed to aid in identifying the mechanism by which anabolic-androgenic << steroids >> (AAS) were activating [[ hAR ]] and potentially interacting with hGR and how glucocorticoid ligands were interacting with the hGR and hAR.


<< Licofelone >>, a balanced inhibitor of [[ cyclooxygenase ]] and 5-lipoxygenase, reduces inflammation in a rabbit model of atherosclerosis.


<< Licofelone >>, a balanced inhibitor of cyclooxygenase and [[ 5-lipoxygenase ]], reduces inflammation in a rabbit model of atherosclerosis.


<< Licofelone >>, a dual anti-inflammatory drug that inhibits 5-lipoxygenase (LOX) and cyclooxygenase (COX) enzymes, may have a better cardiovascular profile that cycloxygenase-2 inhibitors due to [[ cycloxygenase-1 ]] blockade-mediated antithrombotic effect and a better gastrointestinal tolerability.


<< Licofelone >>, a dual anti-inflammatory drug that inhibits [[ 5-lipoxygenase ]] (LOX) and cyclooxygenase (COX) enzymes, may have a better cardiovascular profile that cycloxygenase-2 inhibitors due to cycloxygenase-1 blockade-mediated antithrombotic effect and a better gastrointestinal tolerability.


<< Licofelone >>, a dual anti-inflammatory drug that inhibits 5-lipoxygenase ([[ LOX ]]) and cyclooxygenase (COX) enzymes, may have a better cardiovascular profile that cycloxygenase-2 inhibitors due to cycloxygenase-1 blockade-mediated antithrombotic effect and a better gastrointestinal tolerability.


<< Licofelone >>, a dual anti-inflammatory drug that inhibits 5-lipoxygenase (LOX) and [[ cyclooxygenase ]] (COX) enzymes, may have a better cardiovascular profile that cycloxygenase-2 inhibitors due to cycloxygenase-1 blockade-mediated antithrombotic effect and a better gastrointestinal tolerability.


<< Licofelone >>, a dual anti-inflammatory drug that inhibits 5-lipoxygenase (LOX) and cyclooxygenase ([[ COX ]]) enzymes, may have a better cardiovascular profile that cycloxygenase-2 inhibitors due to cycloxygenase-1 blockade-mediated antithrombotic effect and a better gastrointestinal tolerability.


We examined the anti-inflammatory effect of licofelone on atherosclerotic lesions as well as in isolated neutrophils from whole blood of rabbits compared with a selective inhibitor of << COX-2 >>, [[ rofecoxib ]].


<< Licofelone >> reduced intima/media ratio in injured arteries, the macrophages infiltration in the neointimal area, [[ monocyte chemoattractant protein-1 ]] (MCP-1) gene expression, and the activation of nuclear factor-kappaB in rabbit atheroma.


<< Licofelone >> reduced intima/media ratio in injured arteries, the macrophages infiltration in the neointimal area, monocyte chemoattractant protein-1 ([[ MCP-1 ]]) gene expression, and the activation of nuclear factor-kappaB in rabbit atheroma.


<< Licofelone >> reduced intima/media ratio in injured arteries, the macrophages infiltration in the neointimal area, monocyte chemoattractant protein-1 (MCP-1) gene expression, and the activation of [[ nuclear factor-kappaB ]] in rabbit atheroma.


Moreover, << licofelone >> inhibited [[ COX-2 ]] and 5-LOX protein expression in vascular lesions.


Moreover, << licofelone >> inhibited COX-2 and [[ 5-LOX ]] protein expression in vascular lesions.


<< Rofecoxib >> only diminished [[ COX-2 ]] protein expression and MCP-1 gene expression in vascular atheroma.


<< Rofecoxib >> only diminished COX-2 protein expression and [[ MCP-1 ]] gene expression in vascular atheroma.


<< Licofelone >> almost abolished [[ 5-LOX ]] activity by inhibiting leukotriene B4 generation in rabbit neutrophils and prevented platelet thromboxane B2 production from whole blood.


Licofelone almost abolished << 5-LOX >> activity by inhibiting [[ leukotriene B4 ]] generation in rabbit neutrophils and prevented platelet thromboxane B2 production from whole blood.


Licofelone almost abolished << 5-LOX >> activity by inhibiting leukotriene B4 generation in rabbit neutrophils and prevented platelet [[ thromboxane B2 ]] production from whole blood.


No influence of moderate hepatic impairment on the pharmacokinetics of << lumiracoxib >>, an oral [[ COX-2 ]] selective inhibitor.


The aim of this study was to evaluate the influence of hepatic impairment on the pharmacokinetics (PK) of the novel << cyclooxygenase-2 >> (COX-2) selective inhibitor [[ lumiracoxib ]] (Prexige), so that dose recommendations for clinical use can be provided.


The aim of this study was to evaluate the influence of hepatic impairment on the pharmacokinetics (PK) of the novel cyclooxygenase-2 (<< COX-2 >>) selective inhibitor [[ lumiracoxib ]] (Prexige), so that dose recommendations for clinical use can be provided.


The aim of this study was to evaluate the influence of hepatic impairment on the pharmacokinetics (PK) of the novel << cyclooxygenase-2 >> (COX-2) selective inhibitor lumiracoxib ([[ Prexige ]]), so that dose recommendations for clinical use can be provided.


The aim of this study was to evaluate the influence of hepatic impairment on the pharmacokinetics (PK) of the novel cyclooxygenase-2 (<< COX-2 >>) selective inhibitor lumiracoxib ([[ Prexige ]]), so that dose recommendations for clinical use can be provided.


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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


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