Datasets:

yxchar

/

chemprot-tlm

like 0

<< 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).