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At the enzymatic activity level, << doxycycline >> started to suppress [[ MMP-9 ]] activity at 5 mg/kg/day (P<0.001), while minocycline had an effect at a lower dose, 1 mg/kg/day (P<0.02).

We also assessed the potential relevant signaling pathway in vitro to elucidate the mechanisms underlying the << MMP-9 >> inhibition by [[ tetracyclines ]].

In vitro, << minocycline >>, but not doxycycline, inhibits [[ MMP-9 ]], at least in part, via the extracellular signaling-related kinase 1/2 (ERK1/2)-mediated pathway.

In vitro, minocycline, but not << doxycycline >>, inhibits [[ MMP-9 ]], at least in part, via the extracellular signaling-related kinase 1/2 (ERK1/2)-mediated pathway.

This study provided the evidence that the << tetracyclines >> inhibit stimulated cerebral [[ MMP-9 ]] at multiple levels and are effective at very low doses, offering great potential for therapeutic use.

One major route involves the tetrahydrofolate (THF)-dependent activities of the << glycine decarboxylase complex >> (GDC, EC 2.1.1.10) and serine hydroxymethyltransferase (SHMT, EC 2.1.2.1) with [[ glycine ]] (Gly) as one-carbon (1-C) source.

One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (<< GDC >>, EC 2.1.1.10) and serine hydroxymethyltransferase (SHMT, EC 2.1.2.1) with [[ glycine ]] (Gly) as one-carbon (1-C) source.

One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (GDC, << EC 2.1.1.10 >>) and serine hydroxymethyltransferase (SHMT, EC 2.1.2.1) with [[ glycine ]] (Gly) as one-carbon (1-C) source.

One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (GDC, EC 2.1.1.10) and << serine hydroxymethyltransferase >> (SHMT, EC 2.1.2.1) with [[ glycine ]] (Gly) as one-carbon (1-C) source.

One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (GDC, EC 2.1.1.10) and serine hydroxymethyltransferase (<< SHMT >>, EC 2.1.2.1) with [[ glycine ]] (Gly) as one-carbon (1-C) source.

One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (GDC, EC 2.1.1.10) and serine hydroxymethyltransferase (SHMT, << EC 2.1.2.1 >>) with [[ glycine ]] (Gly) as one-carbon (1-C) source.

One major route involves the tetrahydrofolate (THF)-dependent activities of the << glycine decarboxylase complex >> (GDC, EC 2.1.1.10) and serine hydroxymethyltransferase (SHMT, EC 2.1.2.1) with glycine ([[ Gly ]]) as one-carbon (1-C) source.

One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (<< GDC >>, EC 2.1.1.10) and serine hydroxymethyltransferase (SHMT, EC 2.1.2.1) with glycine ([[ Gly ]]) as one-carbon (1-C) source.

One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (GDC, << EC 2.1.1.10 >>) and serine hydroxymethyltransferase (SHMT, EC 2.1.2.1) with glycine ([[ Gly ]]) as one-carbon (1-C) source.

One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (GDC, EC 2.1.1.10) and << serine hydroxymethyltransferase >> (SHMT, EC 2.1.2.1) with glycine ([[ Gly ]]) as one-carbon (1-C) source.

One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (GDC, EC 2.1.1.10) and serine hydroxymethyltransferase (<< SHMT >>, EC 2.1.2.1) with glycine ([[ Gly ]]) as one-carbon (1-C) source.

One major route involves the tetrahydrofolate (THF)-dependent activities of the glycine decarboxylase complex (GDC, EC 2.1.1.10) and serine hydroxymethyltransferase (SHMT, << EC 2.1.2.1 >>) with glycine ([[ Gly ]]) as one-carbon (1-C) source.

An alternative THF-dependent pathway involves the << C1-THF synthase >>/SHMT activities with [[ formate ]] as 1-C source.

An alternative THF-dependent pathway involves the C1-THF synthase/<< SHMT >> activities with [[ formate ]] as 1-C source.

Firstly, transgenic plants overexpressing << formate dehydrogenase >> (FDH, EC 1.2.1.2) were used to continue our previous studies on the function of FDH in [[ formate ]] metabolism.

Firstly, transgenic plants overexpressing formate dehydrogenase (<< FDH >>, EC 1.2.1.2) were used to continue our previous studies on the function of FDH in [[ formate ]] metabolism.

Firstly, transgenic plants overexpressing formate dehydrogenase (FDH, << EC 1.2.1.2 >>) were used to continue our previous studies on the function of FDH in [[ formate ]] metabolism.

Firstly, transgenic plants overexpressing formate dehydrogenase (FDH, EC 1.2.1.2) were used to continue our previous studies on the function of << FDH >> in [[ formate ]] metabolism.

We concluded that FDH has no direct role in the regulation of the above two pathways of Ser synthesis; the breakdown of formate to << CO(2) >> by the [[ FDH ]] reaction is the primary and preferred fate of the organic acid in Arabidopsis.

We concluded that FDH has no direct role in the regulation of the above two pathways of Ser synthesis; the breakdown of << formate >> to CO(2) by the [[ FDH ]] reaction is the primary and preferred fate of the organic acid in Arabidopsis.

The ratio between the GDC/<< SHMT >> and C1-THF synthase/SHMT pathways of [[ Ser ]] synthesis from [alpha-(13)C]Gly and [(13)C]formate, respectively, in Arabidopsis shoots was 21 : 1; in roots, 9 : 1.

The ratio between the GDC/SHMT and C1-THF synthase/<< SHMT >> pathways of [[ Ser ]] synthesis from [alpha-(13)C]Gly and [(13)C]formate, respectively, in Arabidopsis shoots was 21 : 1; in roots, 9 : 1.

The ratio between the << GDC >>/SHMT and C1-THF synthase/SHMT pathways of Ser synthesis from [[ [alpha-(13)C]Gly ]] and [(13)C]formate, respectively, in Arabidopsis shoots was 21 : 1; in roots, 9 : 1.

The ratio between the GDC/SHMT and << C1-THF synthase >>/SHMT pathways of Ser synthesis from [alpha-(13)C]Gly and [[ [(13)C]formate ]], respectively, in Arabidopsis shoots was 21 : 1; in roots, 9 : 1.

On the other hand, the accumulation of << Ser >> through the C1-THF synthase/[[ SHMT ]] pathway in glyD plants was 2.5-fold greater than that in WT plants.

BACKGROUND: << Rivastigmine >> is a carbamate drug designed to inhibit both [[ acetylcholinesterase ]] and butyrylcholinesterase by reversibly covalently bonding to these enzymes.

BACKGROUND: << Rivastigmine >> is a carbamate drug designed to inhibit both acetylcholinesterase and [[ butyrylcholinesterase ]] by reversibly covalently bonding to these enzymes.

BACKGROUND: Rivastigmine is a << carbamate >> drug designed to inhibit both [[ acetylcholinesterase ]] and butyrylcholinesterase by reversibly covalently bonding to these enzymes.

BACKGROUND: Rivastigmine is a << carbamate >> drug designed to inhibit both acetylcholinesterase and [[ butyrylcholinesterase ]] by reversibly covalently bonding to these enzymes.

<< Topotecan >> is a [[ topoisomerase I ]] inhibitor which is currently evaluated as an adjuvant agent for malignant glioma.

High << p53 >> protein levels, but not genetic or functional p53 status, were associated with increased [[ topotecan ]]-induced DNA/topoisomerase I complex formation.

<< Amiloride >> is a specific inhibitor of [[ uPA ]] but does not inhibit tPA.

The inhibitory effect of endothelin-1 on the contraction induced by 5-HT is abolished by deendothelialization, by the << endothelin ET(B) receptor >> antagonist [[ RES 701-1 ]], by indomethacin, or by glibenclamide.

The potentiation of the contractile effect induced by 5-HT is only somewhat modified by deendothelialization, but abolished by the << thromboxane A2 receptor >> antagonists [[ GR32191 ]] and ridogrel.

The potentiation of the contractile effect induced by 5-HT is only somewhat modified by deendothelialization, but abolished by the << thromboxane A2 receptor >> antagonists GR32191 and [[ ridogrel ]].

A novel class of << quinoxalines >> has been discovered as antagonists of the [[ IgG ]]:FcRn protein-protein interaction through optimization of a hit derived from a virtual ligand-based screen.

A novel class of << quinoxalines >> has been discovered as antagonists of the IgG:[[ FcRn ]] protein-protein interaction through optimization of a hit derived from a virtual ligand-based screen.

<< Agmatine >>, locally synthesized, is an endogenous agonist at [[ imidazoline receptors ]], a noncatecholamine ligand at alpha 2-adrenergic receptors and may act as a neurotransmitter.

(S)-3-(Aminomethyl)-7-(3-hydroxypropoxy)-1-hydroxy-1,3-dihydro-2,1-benzoxaborole (<< GSK2251052 >>) is a novel boron-containing antibiotic that inhibits [[ bacterial leucyl tRNA synthetase ]], and that has been in development for the treatment of serious Gram-negative infections.

<< (S)-3-(Aminomethyl)-7-(3-hydroxypropoxy)-1-hydroxy-1,3-dihydro-2,1-benzoxaborole >> (GSK2251052) is a novel boron-containing antibiotic that inhibits [[ bacterial leucyl tRNA synthetase ]], and that has been in development for the treatment of serious Gram-negative infections.

A combination of in vitro metabolism experiments and a pharmacokinetic study in monkeys with the inhibitor << 4-methylpyrazole >> provided strong evidence that [[ alcohol dehydrogenase ]], potentially in association with aldehyde dehydrogenase, is the primary enzyme involved in the formation of the M3 metabolite.

In functional transport assays, we found that one of the identified molecules, ATM7, increased the reuptake of << serotonin >>, possibly by facilitating the interaction of serotonin with transport-ready conformations of [[ SERT ]] when concentrations of serotonin were low and rate limiting.

In functional transport assays, we found that one of the identified molecules, ATM7, increased the reuptake of serotonin, possibly by facilitating the interaction of << serotonin >> with transport-ready conformations of [[ SERT ]] when concentrations of serotonin were low and rate limiting.

In functional transport assays, we found that one of the identified molecules, ATM7, increased the reuptake of serotonin, possibly by facilitating the interaction of serotonin with transport-ready conformations of << SERT >> when concentrations of [[ serotonin ]] were low and rate limiting.

They display sensitivity to << TK >> inhibitors, including [[ gefitinib ]] and erlotinib.

They display sensitivity to << TK >> inhibitors, including gefitinib and [[ erlotinib ]].

Among the [Fe-S] cluster biosynthetic proteins are included a pyridoxal phosphate-dependent enzyme (<< NifS >>) that is involved in the activation of sulphur from [[ l-cysteine ]], and a molecular scaffold protein (NifU) upon which [Fe-S] cluster precursors are formed.

In addition, the number and area of << glutathione S-transferase placental form >> (GST-P) positive foci and proliferating cell nuclear antigen (PCNA) positive cell ratios in the hepatocytes were significantly increased in the male and female rats that were administered 100mg/kg [[ MEG ]] compared with the control animals.

In addition, the number and area of glutathione S-transferase placental form (<< GST-P >>) positive foci and proliferating cell nuclear antigen (PCNA) positive cell ratios in the hepatocytes were significantly increased in the male and female rats that were administered 100mg/kg [[ MEG ]] compared with the control animals.

In addition, the number and area of glutathione S-transferase placental form (GST-P) positive foci and << proliferating cell nuclear antigen >> (PCNA) positive cell ratios in the hepatocytes were significantly increased in the male and female rats that were administered 100mg/kg [[ MEG ]] compared with the control animals.

In addition, the number and area of glutathione S-transferase placental form (GST-P) positive foci and proliferating cell nuclear antigen (<< PCNA >>) positive cell ratios in the hepatocytes were significantly increased in the male and female rats that were administered 100mg/kg [[ MEG ]] compared with the control animals.

Consumption of << alcohol >> for 8weeks induced severe liver damage with increases in prognostic indicators such as [[ aspartate transaminase ]], alanine transaminase in serum whereas co-administration of CNF suppressed their increases.

Consumption of << alcohol >> for 8weeks induced severe liver damage with increases in prognostic indicators such as aspartate transaminase, [[ alanine transaminase ]] in serum whereas co-administration of CNF suppressed their increases.

Chronic consumption of << alcohol >> also stimulated abrupt increases in pro-inflammatory cytokines such as [[ nuclear factor (NF)-κB ]], tumor necrosis factor (TNF)-α and interleukin (IL)-1β in liver otherwise co-administration of CNF effectively suppressed production of these cytokines dose-dependently.

Chronic consumption of << alcohol >> also stimulated abrupt increases in pro-inflammatory cytokines such as nuclear factor (NF)-κB, [[ tumor necrosis factor (TNF)-α ]] and interleukin (IL)-1β in liver otherwise co-administration of CNF effectively suppressed production of these cytokines dose-dependently.

Chronic consumption of << alcohol >> also stimulated abrupt increases in pro-inflammatory cytokines such as nuclear factor (NF)-κB, tumor necrosis factor (TNF)-α and [[ interleukin (IL)-1β ]] in liver otherwise co-administration of CNF effectively suppressed production of these cytokines dose-dependently.

Dietary << EPA >>/DHA treatment restored endogenous biosynthesis of n-3 derived lipid mediators in obesity while attenuating adipose tissue inflammation and improving [[ insulin ]] sensitivity.

Dietary EPA/<< DHA >> treatment restored endogenous biosynthesis of n-3 derived lipid mediators in obesity while attenuating adipose tissue inflammation and improving [[ insulin ]] sensitivity.

Notably, << 17-HDHA >> treatment reduced adipose tissue expression of inflammatory cytokines, increased [[ adiponectin ]] expression and improved glucose tolerance parallel to insulin sensitivity in obese mice.

Notably, << 17-HDHA >> treatment reduced adipose tissue expression of inflammatory cytokines, increased adiponectin expression and improved glucose tolerance parallel to [[ insulin ]] sensitivity in obese mice.

Notably, << 17-HDHA >> treatment reduced adipose tissue expression of inflammatory [[ cytokines ]], increased adiponectin expression and improved glucose tolerance parallel to insulin sensitivity in obese mice.

Furthermore, we validated the inhibition of << GSK-3β >>/NF-κB signaling following [[ cinobufagin ]] treatment.

Furthermore, we validated the inhibition of GSK-3β/<< NF-κB >> signaling following [[ cinobufagin ]] treatment.

Western blots showed a decrease in nuclear p65 protein expression after exposure to different concentrations of << cinobufagin >>, while the phosphorylation of [[ GSK-3β ]] was simultaneously increased.

Western blots showed a decrease in nuclear << p65 >> protein expression after exposure to different concentrations of [[ cinobufagin ]], while the phosphorylation of GSK-3β was simultaneously increased.

Transduction with constitutively active forms of GSK-3β could protect against the downregulation of p65 and upregulation of cleaved-<< PARP >> that are induced by [[ cinobufagin ]] treatment.

Transduction with constitutively active forms of GSK-3β could protect against the downregulation of << p65 >> and upregulation of cleaved-PARP that are induced by [[ cinobufagin ]] treatment.

However, combined treatment with << cinobufagin >> and SB216367 resulted in a significant reduction in p65 and an increase in cleaved-[[ PARP ]] in U2OS cells.

However, combined treatment with cinobufagin and << SB216367 >> resulted in a significant reduction in p65 and an increase in cleaved-[[ PARP ]] in U2OS cells.

However, combined treatment with << cinobufagin >> and SB216367 resulted in a significant reduction in [[ p65 ]] and an increase in cleaved-PARP in U2OS cells.

However, combined treatment with cinobufagin and << SB216367 >> resulted in a significant reduction in [[ p65 ]] and an increase in cleaved-PARP in U2OS cells.

<< [6]-gingerol >>: a novel [[ AT₁ ]] antagonist for the treatment of cardiovascular disease.

<< [6]-Gingerol >> derived from Zingiber officinale Roscoe (ginger) was identified as a novel [[ angiotensin II type 1 receptor ]] antagonist, with an IC50 value of 8.173 µM.

The major ingredient of ginger, << [6]-gingerol >>, could inhibit [[ angiotensin II type 1 receptor ]] activation, which partially clarified the mechanism of ginger regulating blood pressure and strengthening heart in the cardiovascular system.

In patients who do not reach the LDL-C target, combination therapy with additional << LDL >>-C lowering drugs (e.g. [[ ezetimibe ]], bile acid sequestrants or fibrates) should be considered.

In patients who do not reach the LDL-C target, combination therapy with additional << LDL >>-C lowering drugs (e.g. ezetimibe, [[ bile acid ]] sequestrants or fibrates) should be considered.

In patients who do not reach the LDL-C target, combination therapy with additional << LDL >>-C lowering drugs (e.g. ezetimibe, bile acid sequestrants or [[ fibrates ]]) should be considered.

N(5)-Substituted H(4)biopterin derivatives were not oxidized to products serving as substrates for dihydropteridine reductase and,depending on the substituent, were competitive inhibitors of phenylalanine hydroxylase: << N(5)-methyl >>- and N(5)-hydroxymethyl H(4)biopterin inhibited [[ phenylalanine hydroxylase ]], whereas N(5)-formyl- and N(5)-acetyl H(4)biopterin had no effect.

N(5)-Substituted H(4)biopterin derivatives were not oxidized to products serving as substrates for dihydropteridine reductase and,depending on the substituent, were competitive inhibitors of phenylalanine hydroxylase: N(5)-methyl- and << N(5)-hydroxymethyl H(4)biopterin >> inhibited [[ phenylalanine hydroxylase ]], whereas N(5)-formyl- and N(5)-acetyl H(4)biopterin had no effect.

<< N(5)-Substituted H(4)biopterin >> derivatives were not oxidized to products serving as substrates for [[ dihydropteridine reductase ]] and,depending on the substituent, were competitive inhibitors of phenylalanine hydroxylase: N(5)-methyl- and N(5)-hydroxymethyl H(4)biopterin inhibited phenylalanine hydroxylase, whereas N(5)-formyl- and N(5)-acetyl H(4)biopterin had no effect.

Our data demonstrate differences in the mechanism of stimulation of << phenylalanine hydroxylase >> and nitric oxide synthase by [[ H(4)biopterin ]].

Transfection of the brain cDNA into COS-1 cells resulted in transporter activity that was blocked by the << VMAT >> inhibitor [[ reserpine ]] and a proton ionophore, but not by tetrabenazine, which has a high affinity for VMAT-2.

<< Mitochondrial arginase II >> modulates [[ nitric-oxide ]] synthesis through nonfreely exchangeable L-arginine pools in human endothelial cells.

<< Mitochondrial arginase II >> modulates nitric-oxide synthesis through nonfreely exchangeable [[ L-arginine ]] pools in human endothelial cells.

Reduced synthesis of << nitric oxide >> (NO) contributes to the endothelial dysfunction and may be related to limited availability of L-arginine, the common substrate of [[ constitutive nitric-oxide synthase ]] (NOS) and cytosolic arginase I and mitochondrial arginase II.

Reduced synthesis of << nitric oxide >> (NO) contributes to the endothelial dysfunction and may be related to limited availability of L-arginine, the common substrate of constitutive nitric-oxide synthase ([[ NOS ]]) and cytosolic arginase I and mitochondrial arginase II.

Reduced synthesis of << nitric oxide >> (NO) contributes to the endothelial dysfunction and may be related to limited availability of L-arginine, the common substrate of constitutive nitric-oxide synthase (NOS) and cytosolic [[ arginase I ]] and mitochondrial arginase II.

Reduced synthesis of << nitric oxide >> (NO) contributes to the endothelial dysfunction and may be related to limited availability of L-arginine, the common substrate of constitutive nitric-oxide synthase (NOS) and cytosolic arginase I and [[ mitochondrial arginase II ]].

Reduced synthesis of nitric oxide (<< NO >>) contributes to the endothelial dysfunction and may be related to limited availability of L-arginine, the common substrate of [[ constitutive nitric-oxide synthase ]] (NOS) and cytosolic arginase I and mitochondrial arginase II.

Reduced synthesis of nitric oxide (<< NO >>) contributes to the endothelial dysfunction and may be related to limited availability of L-arginine, the common substrate of constitutive nitric-oxide synthase ([[ NOS ]]) and cytosolic arginase I and mitochondrial arginase II.

Reduced synthesis of nitric oxide (<< NO >>) contributes to the endothelial dysfunction and may be related to limited availability of L-arginine, the common substrate of constitutive nitric-oxide synthase (NOS) and cytosolic [[ arginase I ]] and mitochondrial arginase II.

Reduced synthesis of nitric oxide (<< NO >>) contributes to the endothelial dysfunction and may be related to limited availability of L-arginine, the common substrate of constitutive nitric-oxide synthase (NOS) and cytosolic arginase I and [[ mitochondrial arginase II ]].

Reduced synthesis of nitric oxide (NO) contributes to the endothelial dysfunction and may be related to limited availability of << L-arginine >>, the common substrate of [[ constitutive nitric-oxide synthase ]] (NOS) and cytosolic arginase I and mitochondrial arginase II.

Reduced synthesis of nitric oxide (NO) contributes to the endothelial dysfunction and may be related to limited availability of << L-arginine >>, the common substrate of constitutive nitric-oxide synthase ([[ NOS ]]) and cytosolic arginase I and mitochondrial arginase II.

Reduced synthesis of nitric oxide (NO) contributes to the endothelial dysfunction and may be related to limited availability of << L-arginine >>, the common substrate of constitutive nitric-oxide synthase (NOS) and cytosolic [[ arginase I ]] and mitochondrial arginase II.