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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). | INHIBITOR | [] |
We also assessed the potential relevant signaling pathway in vitro to elucidate the mechanisms underlying the << MMP-9 >> inhibition by [[ tetracyclines ]]. | INHIBITOR | [] |
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. | INHIBITOR | [] |
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. | INHIBITOR | [] |
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. | INHIBITOR | [] |
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. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |
An alternative THF-dependent pathway involves the << C1-THF synthase >>/SHMT activities with [[ formate ]] as 1-C source. | SUBSTRATE | [] |
An alternative THF-dependent pathway involves the C1-THF synthase/<< SHMT >> activities with [[ formate ]] as 1-C source. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |
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. | PRODUCT-OF | [] |
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. | SUBSTRATE | [] |
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. | PRODUCT-OF | [] |
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. | PRODUCT-OF | [] |
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. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |
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. | PRODUCT-OF | [] |
BACKGROUND: << Rivastigmine >> is a carbamate drug designed to inhibit both [[ acetylcholinesterase ]] and butyrylcholinesterase by reversibly covalently bonding to these enzymes. | INHIBITOR | [] |
BACKGROUND: << Rivastigmine >> is a carbamate drug designed to inhibit both acetylcholinesterase and [[ butyrylcholinesterase ]] by reversibly covalently bonding to these enzymes. | INHIBITOR | [] |
BACKGROUND: Rivastigmine is a << carbamate >> drug designed to inhibit both [[ acetylcholinesterase ]] and butyrylcholinesterase by reversibly covalently bonding to these enzymes. | INHIBITOR | [] |
BACKGROUND: Rivastigmine is a << carbamate >> drug designed to inhibit both acetylcholinesterase and [[ butyrylcholinesterase ]] by reversibly covalently bonding to these enzymes. | INHIBITOR | [] |
<< Topotecan >> is a [[ topoisomerase I ]] inhibitor which is currently evaluated as an adjuvant agent for malignant glioma. | INHIBITOR | [] |
High << p53 >> protein levels, but not genetic or functional p53 status, were associated with increased [[ topotecan ]]-induced DNA/topoisomerase I complex formation. | INDIRECT-UPREGULATOR | [] |
<< Amiloride >> is a specific inhibitor of [[ uPA ]] but does not inhibit tPA. | INHIBITOR | [] |
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. | ANTAGONIST | [] |
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. | ANTAGONIST | [] |
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 ]]. | ANTAGONIST | [] |
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. | ANTAGONIST | [] |
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. | ANTAGONIST | [] |
<< Agmatine >>, locally synthesized, is an endogenous agonist at [[ imidazoline receptors ]], a noncatecholamine ligand at alpha 2-adrenergic receptors and may act as a neurotransmitter. | AGONIST | [] |
(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. | INHIBITOR | [] |
<< (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. | INHIBITOR | [] |
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. | INHIBITOR | [] |
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. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |
They display sensitivity to << TK >> inhibitors, including [[ gefitinib ]] and erlotinib. | INHIBITOR | [] |
They display sensitivity to << TK >> inhibitors, including gefitinib and [[ erlotinib ]]. | INHIBITOR | [] |
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. | SUBSTRATE | [] |
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. | INDIRECT-UPREGULATOR | [] |
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. | INDIRECT-UPREGULATOR | [] |
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. | INDIRECT-UPREGULATOR | [] |
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. | INDIRECT-UPREGULATOR | [] |
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. | INDIRECT-UPREGULATOR | [] |
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. | INDIRECT-UPREGULATOR | [] |
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. | ACTIVATOR | [] |
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. | ACTIVATOR | [] |
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. | ACTIVATOR | [] |
Dietary << EPA >>/DHA treatment restored endogenous biosynthesis of n-3 derived lipid mediators in obesity while attenuating adipose tissue inflammation and improving [[ insulin ]] sensitivity. | INDIRECT-UPREGULATOR | [] |
Dietary EPA/<< DHA >> treatment restored endogenous biosynthesis of n-3 derived lipid mediators in obesity while attenuating adipose tissue inflammation and improving [[ insulin ]] sensitivity. | INDIRECT-UPREGULATOR | [] |
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. | INDIRECT-UPREGULATOR | [] |
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. | INDIRECT-UPREGULATOR | [] |
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. | INDIRECT-DOWNREGULATOR | [] |
Furthermore, we validated the inhibition of << GSK-3β >>/NF-κB signaling following [[ cinobufagin ]] treatment. | INDIRECT-DOWNREGULATOR | [] |
Furthermore, we validated the inhibition of GSK-3β/<< NF-κB >> signaling following [[ cinobufagin ]] treatment. | INDIRECT-DOWNREGULATOR | [] |
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. | ACTIVATOR | [] |
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. | INDIRECT-DOWNREGULATOR | [] |
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. | INDIRECT-UPREGULATOR | [] |
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. | INDIRECT-DOWNREGULATOR | [] |
However, combined treatment with << cinobufagin >> and SB216367 resulted in a significant reduction in p65 and an increase in cleaved-[[ PARP ]] in U2OS cells. | INDIRECT-UPREGULATOR | [] |
However, combined treatment with cinobufagin and << SB216367 >> resulted in a significant reduction in p65 and an increase in cleaved-[[ PARP ]] in U2OS cells. | INDIRECT-UPREGULATOR | [] |
However, combined treatment with << cinobufagin >> and SB216367 resulted in a significant reduction in [[ p65 ]] and an increase in cleaved-PARP in U2OS cells. | INDIRECT-DOWNREGULATOR | [] |
However, combined treatment with cinobufagin and << SB216367 >> resulted in a significant reduction in [[ p65 ]] and an increase in cleaved-PARP in U2OS cells. | INDIRECT-DOWNREGULATOR | [] |
<< [6]-gingerol >>: a novel [[ AT₁ ]] antagonist for the treatment of cardiovascular disease. | ANTAGONIST | [] |
<< [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. | ANTAGONIST | [] |
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. | INHIBITOR | [] |
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. | INHIBITOR | [] |
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. | INHIBITOR | [] |
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. | INHIBITOR | [] |
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. | INHIBITOR | [] |
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. | INHIBITOR | [] |
<< 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. | SUBSTRATE | [] |
Our data demonstrate differences in the mechanism of stimulation of << phenylalanine hydroxylase >> and nitric oxide synthase by [[ H(4)biopterin ]]. | INHIBITOR | [] |
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. | INHIBITOR | [] |
<< Mitochondrial arginase II >> modulates [[ nitric-oxide ]] synthesis through nonfreely exchangeable L-arginine pools in human endothelial cells. | PRODUCT-OF | [] |
<< Mitochondrial arginase II >> modulates nitric-oxide synthesis through nonfreely exchangeable [[ L-arginine ]] pools in human endothelial cells. | SUBSTRATE | [] |
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. | PRODUCT-OF | [] |
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. | PRODUCT-OF | [] |
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. | PRODUCT-OF | [] |
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 ]]. | PRODUCT-OF | [] |
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. | PRODUCT-OF | [] |
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. | PRODUCT-OF | [] |
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. | PRODUCT-OF | [] |
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 ]]. | PRODUCT-OF | [] |
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. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |
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. | SUBSTRATE | [] |