EC Number   |
Recommended Name  |
Application |
|---|
    2.5.1.10 | (2E,6E)-farnesyl diphosphate synthase |
medicine |
chronic treatment with an FPPS inhibitor attenuates the development of cardiac hypertrophy and fibrosis |
| 2.5.1.10 | (2E,6E)-farnesyl diphosphate synthase |
medicine |
shRNA-mediated knock-down of expression results in conversion of hematopoietic and nonhematopoietic tumor cell lines into Vgamma9Vdelta2 T-cell activators. Knock-down cells activate Vgamma9Vdelta2 cells. Vgamma9Vdelta2 cells act as sensors of a dysregulated isoprenoid metabolism, therapeutic down-modulation of FPPS expression may be used as a tool to target tumor cells to Vgamma9Vdelta2 T-cell mediated immunosurveillance |
| 2.5.1.10 | (2E,6E)-farnesyl diphosphate synthase |
medicine |
the enzyme is a target for Chagas disease chemotherapy |
| 2.4.1.92 | (N-acetylneuraminyl)-galactosylglucosylceramide N-acetylgalactosaminyltransferase |
medicine |
GD2 synthase is a surface marker for the identification of mesenchymal stromal cells |
| 2.4.1.92 | (N-acetylneuraminyl)-galactosylglucosylceramide N-acetylgalactosaminyltransferase |
medicine |
GD2/GM2 synthase mRNA is not a reliable biomarker for small cell lung cancer |
| 2.3.3.21 | (R)-citramalate synthase |
medicine |
catalyses the first reaction of the pathway which converts pyruvate and acetyl-CoA into citramalate, thus making it an attractive target for the development of antibacterial agents |
| 2.3.3.21 | (R)-citramalate synthase |
medicine |
Leptospira interrogans is the causative agent for leptospirosis, LiCMS is an atttractive target for the development of antibacterial agents |
| 2.1.1.128 | (RS)-norcoclaurine 6-O-methyltransferase |
medicine |
a Saccharomyces cerevisiae strain is engineered to express seven heterologous enzymes (Papaper somniferum norcoclaurine 6-O-methyltransferase (Ps6OMT), Papaver somniferum 3'-hydroxy-N-methylcoclaurine 4'-O-methyltransferase 2 (Ps4'OMT), Papapver somniferum coclaurine N-methyltransferase (PsCNMT), Papaver somniferum berberine bridge enzyme (PsBBE), Thalictrum flavum scoulerine 9-O-methyltransferase (TfS9OMT), Thalictrum flavum canadine synthase (TfCAS), and Arabidopsis thaliana cytochrome P450 reductase 1 (CPR)), resulting in protoberberine alkaloid production from a simple benzylisoquinoline alkaloid precursor. A number of strategies are implemented to improve flux through the pathway, including enzyme variant screening, genetic copy number variation, and culture optimization. This leads to an over 70-fold increase in canadine titer up to 1.8 mg/l. Increased canadine titers enable extension of the pathway to produce berberine, a major constituent of several traditional medicines in a microbial host. This strain is viable at pilot scale |
| 1.1.3.15 | (S)-2-hydroxy-acid oxidase |
medicine |
enzyme is used in clinical chemistry for the determination of (S)-lactate in blood in some pathological diseases such as diabetes, heart diseases and shock syndrome |
| 1.1.3.15 | (S)-2-hydroxy-acid oxidase |
medicine |
decrease of enzyme activity upon oxidative stress induced by glutathione depletion or postischemic perfusion, down-regulation of enzyme as mechanism to prevent excessive H2O2 formation in liver peroxisome |
| 1.1.3.15 | (S)-2-hydroxy-acid oxidase |
medicine |
the ability of such siRNAs to reduce urinary oxalate in the mouse model suggests that this approach is promising for the treatment of primary hyperoxalurias, PH, particularly PH type I, in humans, genes HYPDH and GO appear to be the best targets for reducing the production of glyoxylate and oxalate in PH patients |
| 1.1.3.15 | (S)-2-hydroxy-acid oxidase |
medicine |
application of oan in vivo CRISPR/Cas9-mediated substrate reduction therapy to treat primary hyperoxaluria type I that results in excessive hepatic oxalate production causing end-stage renal disease. A single systemic administration of an AAV8-CRISPR/Cas9 vector targeting glycolate oxidase, prevents oxalate overproduction and kidney damage, with no signs of toxicity in Agxt1-/- mice |
| 1.1.5.13 | (S)-2-hydroxyglutarate dehydrogenase |
medicine |
lower enzyme expression is associated with tumor progression and/or worsened prognosis in patients with renal cell carcinoma |
| 1.11.1.23 | (S)-2-hydroxypropylphosphonic acid epoxidase |
medicine |
fosfomycin is a clinically useful antibiotic for the treatment of limb-threatening diabetic foot infections and lower urinary tract infections. It is effective against ciprofloxacin-resistant Escherichia coli, as well as methicillin-resistant and vancomycin-resistant strains of Staphylococcus aureus. The antimicrobial activity of fosfomycin is due to the inactivation of UDP-GlcNAc-3-O-enolpyruvyltransferase, which catalyzes the first committed step in the biosynthesis of peptidoglycan, the main component of the bacterial cell wall |
| 1.11.1.23 | (S)-2-hydroxypropylphosphonic acid epoxidase |
medicine |
fosfomycin is a clinically utilized antibiotic of low toxicity, blocking bacterial cell wall biosynthesis by acting as an analogue of phosphoenolpyruvate |
| 1.14.19.68 | (S)-canadine synthase |
medicine |
a Saccharomyces cerevisiae strain is engineered to express seven heterologous enzymes (Papaper somniferum norcoclaurine 6-O-methyltransferase (Ps6OMT), Papaver somniferum 3'-hydroxy-N-methylcoclaurine 4'-O-methyltransferase 2 (Ps4'OMT), Papapver somniferum coclaurine N-methyltransferase (PsCNMT), Papaver somniferum berberine bridge enzyme (PsBBE), Thalictrum flavum scoulerine 9-O-methyltransferase (TfS9OMT), Thalictrum flavum canadine synthase (TfCAS), and Arabidopsis thaliana cytochrome P450 reductase 1 (CPR)), resulting in protoberberine alkaloid production from a simple benzylisoquinoline alkaloid precursor. A number of strategies are implemented to improve flux through the pathway, including enzyme variant screening, genetic copy number variation, and culture optimization. This leads to an over 70-fold increase in canadine titer up to 1.8 mg/l. Increased canadine titers enable extension of the pathway to produce berberine, a major constituent of several traditional medicines in a microbial host. This strain is viable at pilot scale |
| 2.1.1.140 | (S)-coclaurine-N-methyltransferase |
medicine |
a Saccharomyces cerevisiae strain is engineered to express seven heterologous enzymes (Papaper somniferum norcoclaurine 6-O-methyltransferase (Ps6OMT), Papaver somniferum 3'-hydroxy-N-methylcoclaurine 4'-O-methyltransferase 2 (Ps4'OMT), Papapver somniferum coclaurine N-methyltransferase (PsCNMT), Papaver somniferum berberine bridge enzyme (PsBBE), Thalictrum flavum scoulerine 9-O-methyltransferase (TfS9OMT), Thalictrum flavum canadine synthase (TfCAS), and Arabidopsis thaliana cytochrome P450 reductase 1 (CPR)), resulting in protoberberine alkaloid production from a simple benzylisoquinoline alkaloid precursor. A number of strategies are implemented to improve flux through the pathway, including enzyme variant screening, genetic copy number variation, and culture optimization. This leads to an over 70-fold increase in canadine titer up to 1.8 mg/l. Increased canadine titers enable extension of the pathway to produce berberine, a major constituent of several traditional medicines in a microbial host. This strain is viable at pilot scale |
| 2.1.1.117 | (S)-scoulerine 9-O-methyltransferase |
medicine |
a Saccharomyces cerevisiae strain is engineered to express seven heterologous enzymes (Papaper somniferum norcoclaurine 6-O-methyltransferase (Ps6OMT), Papaver somniferum 3'-hydroxy-N-methylcoclaurine 4'-O-methyltransferase 2 (Ps4'OMT), Papapver somniferum coclaurine N-methyltransferase (PsCNMT), Papaver somniferum berberine bridge enzyme (PsBBE), Thalictrum flavum scoulerine 9-O-methyltransferase (TfS9OMT), Thalictrum flavum canadine synthase (TfCAS), and Arabidopsis thaliana cytochrome P450 reductase 1 (CPR)), resulting in protoberberine alkaloid production from a simple benzylisoquinoline alkaloid precursor. A number of strategies are implemented to improve flux through the pathway, including enzyme variant screening, genetic copy number variation, and culture optimization. This leads to an over 70-fold increase in canadine titer up to 1.8 mg/l. Increased canadine titers enable extension of the pathway to produce berberine, a major constituent of several traditional medicines in a microbial host. This strain is viable at pilot scale |
| 3.2.1.63 | 1,2-alpha-L-fucosidase |
medicine |
1,2-alpha-L-fucosynthase, derived from an inverting alpha-glycosidase (AfcA) and from a glycosidase with an unusual reaction mechanism, may serve as a promising tool to create biologically active compounds that can be used not only for prebiotics but also for clinical treatments aimed to regulate various cellular processes and infectious diseases |
| 2.4.1.211 | 1,3-beta-galactosyl-N-acetylhexosamine phosphorylase |
medicine |
galactosyl-N-acetylhexosamine phosphorylase has a predominant role in the digestive tract of human and in the metabolism of galactose |
| 2.4.1.34 | 1,3-beta-glucan synthase |
medicine |
exposure of strain RG101 to caspofungin during growth yields a modified enzyme that is drug insensitive (4 log orders) in kinetic inhibition assays, and this insensitivity is also observed for enzymes isolated from clinical isolates. The lipid microenvironment of the enzyme with resistance induced by caspofungin reveals a prominent increase in the abundances of dihydrosphingosine and phytosphingosine. Exogenous addition of dihydrosphingosine and phytosphingosine to the sensitive enzyme recapitulates the drug insensitivity of the caspofungin-derived enzyme. Caspofungin induces mitochondrion-derived reactive oxygen species, and dampening reactive oxygen species formation by antimycin A or thiourea eliminates drug-induced resistance |
| 2.4.1.18 | 1,4-alpha-glucan branching enzyme |
medicine |
defining the molecular basis of equine glycogen storage disease IV will allow for accurate DNA testing and the ability to prevent occurence of this disease affecting American Quarter Horses and related breeds. A C to A substitution at base 102 results in a tyrosine (Y) to stop (X) mutation in codon 34 of exon of exon 1. All 11 affected foals are homozygous for the X34 allele, all 16 control horses are homozygous for the Y34 allele |
| 4.1.3.36 | 1,4-dihydroxy-2-naphthoyl-CoA synthase |
medicine |
mutations in the menB gene, the gene encoding naphthoate synthase, cause the small-colony variant phenotype, small-colony variants are associated with persistent infections and may be selectively enriched during antibody therapy |
| 3.1.1.25 | 1,4-lactonase |
medicine |
PON1 overexpression is associated with decreased diabetes-induced macrophage oxidative stress, decreased diabetes development, and decreased mortality |
| 3.1.1.25 | 1,4-lactonase |
medicine |
incubation of serum or high density lipoprotein from healthy subjects with very low density lipoprotein significantly decreases serum paraoxonase 1 lactonase or arylesterase activities by up to 11% or 24%, and HDL-associated paraoxonase 1 lactonase or arylesterase activities by up to 32% or 46%, respectively. Very low density lipoprotein also inhibits recombinant paraoxonase 1 lactonase or arylesterase activities by up to 20% or 42%, respectively. Bezafibrate therapy to three hypertriglyceridemic patients (400 mg/day, for one month) significantly decreased serum triglyceride concentration by 67%, and increased serum high density lipoproteincholesterol levels by 48%. Paraoxonase 1 arylesterase or paraoxonase activities in the patients' high density lipoprotein fractions after drug therapy are significantly increased by 86-88%, as compared to paraoxonase 1 activities before treatment. High density lipoprotein-paraoxonase 1 protein levels significantly increased after bezafibrate therapy |
| 3.2.1.127 | 1,6-alpha-L-fucosidase |
medicine |
progression-free survival significantly longer in high FUCA activity group than in low FUCA activity group, not correlated to clinical response to trastuzumab but maybe useful as biomarker for predicting progression-free survival for trastuzumab treatment |
| 3.2.1.127 | 1,6-alpha-L-fucosidase |
medicine |
using BfFucH coupled with endoglycosidases and the emerging glycosynthases allows glycoengineering of IgG antibodies to provide homogeneous glycoforms with well-defined glycan structures and optimal effector function |
| 2.3.1.51 | 1-acylglycerol-3-phosphate O-acyltransferase |
medicine |
expression of isoform AGPAT11 mRNA is signifi cantly upregulated in human breast, cervical, and colorectal cancer tissues |
| 2.3.1.51 | 1-acylglycerol-3-phosphate O-acyltransferase |
medicine |
expression of isoform CGI-58 in fibroblasts from humans with Chanarin-Dorfman increases the incorporation of fatty acids released from the lipolysis of stored triacylglycerols into phospholipids |
| 2.3.1.51 | 1-acylglycerol-3-phosphate O-acyltransferase |
medicine |
expression of isoform LPAATbeta is readily detected in 8 of 10 analyzed human osteosarcoma lines. Exogenous expression of LPAATbeta promotes osteosarcoma cell proliferation and migration, while silencing LPAATbeta expression inhibits these cellular characteristics. Exogenous expression of LPAATbeta effectively promotes tumor growth, while knockdown of LPAATbeta expression inhibits tumor growth in an orthotopic xenograft model of human osteosarcoma |
| 2.3.1.51 | 1-acylglycerol-3-phosphate O-acyltransferase |
medicine |
the role of isoforms AGPAT1 or AGPAT2 in liver lipogenesis is minimal and accumulation of liver fat is primarily a consequence of insulin resistance and loss of adipose tissue in Agpat2 -/- mice |
| 2.3.1.23 | 1-acylglycerophosphocholine O-acyltransferase |
medicine |
LPCAT3 may have potential as a therapeutic target for diseases, including atherosclerosis, non-alcoholic steatohepatitis, and carcinoma |
| 3.1.1.47 | 1-alkyl-2-acetylglycerophosphocholine esterase |
medicine |
the gene for the beta subunit of brain enzyme isoform I is identical to a causative gene for Miller-Dieker lissencephaly |
| 3.1.1.47 | 1-alkyl-2-acetylglycerophosphocholine esterase |
medicine |
plasma isozyme is a target of many clinical studies in inflammatory diseases, such as asthma, sepsis, and vascular diseases |
| 3.1.1.47 | 1-alkyl-2-acetylglycerophosphocholine esterase |
medicine |
recombinant plasma enzyme form can prevent or attenuate pathological inflammation in a number of animal models, it may have pharmacological potential in human inflammatory disease as well, overview |
| 3.1.1.47 | 1-alkyl-2-acetylglycerophosphocholine esterase |
medicine |
potential use of PAF-AH alpha2 as pharmacologically active protein to promote cell survival |
| 3.1.1.47 | 1-alkyl-2-acetylglycerophosphocholine esterase |
medicine |
in human neither in asthma nor in sepsis the recombinant enzyme shows sufficient efficiacy. In numerous animal models of inflammation or sepsis rPAF-AH is efficient, pointing out the extreme difficulty to extrapolate from small animal models to human beings |
| 3.1.1.47 | 1-alkyl-2-acetylglycerophosphocholine esterase |
medicine |
PAF-AH II exerts strong neuroprotective effects against ischemic injury. This results suggest a possibility for clinical use of this enzyme in cerebral ischemia |
| 3.1.1.47 | 1-alkyl-2-acetylglycerophosphocholine esterase |
medicine |
the use of PAF inactivator enhances the livers recovery from paracetamol intoxication and attenuates the severity of experimental liver injury, providing important means of improving liver function following paracetamol intoxication |
| 3.1.1.47 | 1-alkyl-2-acetylglycerophosphocholine esterase |
medicine |
an altered location of PAF-AH correlates with diseases such as coronary artery disease, hypercholesterolemia, paroxysmal atrial fibrillation and chronic kidney disease |
| 3.1.1.47 | 1-alkyl-2-acetylglycerophosphocholine esterase |
medicine |
elevated Lp-PLA2 levels are correlated to increased risk for cardiovascular events |
| 3.1.1.47 | 1-alkyl-2-acetylglycerophosphocholine esterase |
medicine |
lipoprotein associated phospholipase A2 is a cardiovascular risk marker, in addition, its inhibition reduces the generation of oxidized fatty acids |
| 3.1.1.47 | 1-alkyl-2-acetylglycerophosphocholine esterase |
medicine |
lipoprotein-associated phospholipase A2 is a biomarker that can be used to assess the risk for cardiovascular disease and events, in addition several studies suggest that the enzyme has a pathological role in the atherosclerotic disease process |
| 3.1.1.47 | 1-alkyl-2-acetylglycerophosphocholine esterase |
medicine |
lipoprotein-associated phospholipase A2 is among the multiple cardiovascular biomarkers that have been associated with increased cardiovascular disease risk |
| 3.1.1.47 | 1-alkyl-2-acetylglycerophosphocholine esterase |
medicine |
lipoprotein-associated phospholipase A2 is an emerging risk factor for cardiovascular disease |
| 3.1.1.47 | 1-alkyl-2-acetylglycerophosphocholine esterase |
medicine |
plasma platelet activating factor acetylhydrolase functions as a general anti-inflammatory scavenger by reducing the levels of the signaling molecule platelet activating factor |
| 3.1.1.47 | 1-alkyl-2-acetylglycerophosphocholine esterase |
medicine |
serum platelet-activating factor acetylhydrolase is a potential inflammatory marker in type 1 diabetes |
| 2.3.1.67 | 1-alkylglycerophosphocholine O-acetyltransferase |
medicine |
metabolic role in inflammatory disorders using experimental allergic encephalomyelitis (EAE), an animal model for multiple sclerosis (MS) |
| 2.3.1.67 | 1-alkylglycerophosphocholine O-acetyltransferase |
medicine |
the results increases the understanding of the clinical implications of platelet-activating factor inhibition with regard to HIV infection |
| 2.3.1.67 | 1-alkylglycerophosphocholine O-acetyltransferase |
medicine |
inhibitors 3-decanoyloxy-2-methoxy-5-methyl-1,4-benzoquinone and 2-methoxy-5-methyl-3-tetradecanoyloxy-1,4-benzoquinone at 2.5 mg/kg shod significant, 47.9-51.7%, inhibition in the carrageenan-induced mouse paw edema test, stronger than that of prednisolone at 10 mg/kg |
| 2.3.1.67 | 1-alkylglycerophosphocholine O-acetyltransferase |
medicine |
study on the impact of diet on platelet-activating factor metabolism. Platelet-activating factor is inversely correlated with antioxidant-rich foods (herbal drinks and coffee), the dietary antioxidant capacity as well as a dietary pattern characterized by legumes, vegetables, poultry and fish. Platelet-activating factor is positively correlated to percentage of fat intake. Lyso-PAF acetyltransferase is also negatively associated with healthy patterns (fruits, nuts and herbal drinks, and a pattern rich in olive oil and whole-wheat products), as well as the dietary antioxidant capacity and percentage of monounsaturated fatty acids |
| 1.1.1.267 | 1-deoxy-D-xylulose-5-phosphate reductoisomerase |
medicine |
50% inhibition of growth of parasite in cultured infected erythrocytes is 2-3 times lower with fetal bovine serum in the culture liquide than with human serum |
| 1.1.1.267 | 1-deoxy-D-xylulose-5-phosphate reductoisomerase |
medicine |
study on inhibitory effect of antimalarial drugs in clinical isolates of Plasmodium falciparum. No correlation between chloroquine or pyrimethamine and fosmidomycin. Fosmidomycin is moderately active against both chloroquine-susceptible and chloroquine-resistant isolates |
| 2.2.1.7 | 1-deoxy-D-xylulose-5-phosphate synthase |
medicine |
development of 1-deoxy-D-xylulose-5-phosphate synthase inhibitors to treat Plasmodium vivax malaria |
| 2.7.1.67 | 1-phosphatidylinositol 4-kinase |
medicine |
PI4Ks are panviral host therapeutic targets |
| 2.7.1.149 | 1-phosphatidylinositol-5-phosphate 4-kinase |
medicine |
phosphatidylinositol-5-phosphate 4-kinase type II beta might be an effective therapeutic target for preventing of colon cancer progression |
| 2.4.1.277 | 10-deoxymethynolide desosaminyltransferase |
medicine |
the catalytic flexibility of the glycosyltransferase DesVII offers an means for creating new macrolide antibiotics. The substrate flexibility of DesVII/DesVIII is apparently extended to a wide range of linear as well as cyclic substrates. Although the yield of products is notably reduced when unnatural substrates are used, once a desired activity is identified, the catalytic efficiency of these enzymes may be fine-tuned by protein engineering. The substrate flexibility of glycosyltransferases expands the opportunities for glycodiversification to generate new glycoforms of synthetic compounds and macrolide analogues |
| 2.4.1.277 | 10-deoxymethynolide desosaminyltransferase |
medicine |
the requirement for an additional protein component, DesVIII, for activity must be taken into consideration in the design of combinatorial biosynthetic experiments with new glycosylated macrolides |
| 1.1.1.315 | 11-cis-retinol dehydrogenase |
medicine |
evaluation of patients with hereditary retinal diseases featuring subretinal spots, i.e. retinitis punctata albescens and fundus albipunctatus, and patients with typical dominant or recessive retinitis pigmentosa for mutations in RDH5. Mutations are found only in two unrelated patients, both with fundus albipunctatus. Mutations segregate with disease in the respective families. Recombinant mutant 11-cis retinol dehydrogenases have reduced activity compared with recombinant enzyme with wild-type sequence |
| 1.1.1.315 | 11-cis-retinol dehydrogenase |
medicine |
examination of two unrelated families, each family with two affected members with typical fundus albipunctatus. RDH5 mutations were found in the affected siblings in both families. The proband in one has a homozygotic Gly238Trp missense mutation (GGG to TGG) involving exon 4 and in the other carries compound heterozygotic changes Arg280His (CGC to CAC) and Ala294Pro (GCC to CCC) in exon 5. The disease phenotype is only manifested in family members with two abnormal RDH5 alleles consistent with autosomal recessive inheritance in both pedigrees |
| 1.1.1.315 | 11-cis-retinol dehydrogenase |
medicine |
mutations in gene RDH5 are associated with fundus albipunctatus, an autosomal recessive eye disease. Characterization of 11 mutants shows that all RDH5 mutants show decreased protein stability and subcellular mislocalization and, in most cases, loss of enzymatic activity in vitro and in vivo. The mutated enzymes, in a transdominant-negative manner, influence the in vivo enzymatic properties of functional variants of the enzyme. Under certain conditions, nonfunctional alleles act in a dominant-negative way on functional but relatively unstable mutated alleles. In heterozygous individuals carrying one wild-type allele, the disease is recessive, probably due to the stability of the wild-type enzyme |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
exposure of fetus to high levels of synthetic glucocorticoid may have long-lasting effects on the hippocampal expression of hypothalamic-pituitary-adrenal-related genes into adulthood |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
high-fat diet-induced obesity is accompanied by increased visceral fat preadipocyte differentiation in wild-type but not 11beta-HSD1 -/- mice |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
methionine restriction disrupts the lipogenic/lipolytic balance, contributing importantly to adiposity resistance in Fischer 344 rats |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
treatment of rats with dehydroepiandrosterone induces a shift from isoform 11beta-HSD1 to 11beta-HSD2 expression, increasing conversion from active to inactive glucocorticoids |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
activation of cortisol by 11beta-hydroxysteroid dehydrogenase in granulosa cells increases with follicle development but is significantly decreased in ovarion cysts |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
changes in ovarian cortisol metabolism are accompanied by corresponding changes in the levels of paracrine inhibitors of 11beta-hydroxysteroid dehydrogenase within growing ovarian follicles and cysts |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
differentiation of cells causes a strong increase in 11beta-hydroxysteroid dehydrogenase protein levels, occuring late in the differentiation protocol. Reduction of 11beta-hydroxysteroid dehydrogenase activity in 3T3-L1 fibroblasts, achieved by pharmacological inhibition or adenovirally mediated delivery of short hairpin RNA constructs, specifically blocks the ability of inactive glucocorticoids to drive 3T3-L1 differentiation. Even modest increases in exogenous 11beta-hydroxysteroid dehydrogenase expression in 3T3-L1 fibroblasts, to levels comparable with endogenous 1 11beta-hydroxysteroid dehydrogenase in differentiated 3T3-L1 adipocytes, are sufficient to block adipogenesis |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
in morbidly obese patients, 11beta-hydroxysteroid dehydrogenase 1 mRNA levlels are higher in subcutaneous adipose tissue than in visceral adipose tissue. Subcutaneous adipose tissue 11beta-hydroxysteroid dehydrogenase 1 levels increase parallel according to body mass index category. No correlation between subcutaneous adipose tissue or visceral adipose tissue with fasting glucose, total cholesterol, triglycerides, and high-density lipoprotein |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
inhibition of 11beta-hydroxysteroid dehydrogenase type 1 activity reduces the availability of cortisol to activate the glucocorticoid receptor, down regulates gluconeogenesis and thus reduces plasma glucose levels in cortisone-induced diabetic KK mice. In mice treated with 11beta-hydroxysteroid dehydrogenase type 1-antisense oligonucleotide, plasma blood glucose levels are significantly reduced by up to 54% upon induction of diabetes. Cortisol and other diabetes end products are also reduced, and hepatic 11beta-hydroxysteroid dehydrogenase type 1 mRNA is suppressed by up to 84% |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
significant decrease in 11beta-hydroxysteroid dehydrogenase reductase activity in mice with glycogen storage disease type 1b, whereas mice with glycogen storage disease type 1a show a marked increase in enzyme activity |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
significant decrease in 11beta-hydroxysteroid dehydrogenase reductase activity in patients with glycogen storage disease type 1b, whereas patients with glycogen storage disease type 1a show a marked increase in enzyme activity |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
significant induction of 11beta-hydroxysteroid dehydrogenase type 1 gene expression and activity in patients with alcoholic liver disease during long-term and short-term abstinence from alcohol |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
sucrose can promote increased 11beta-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase message in mesenteric fat while concomitantly decreasing 11beta-dehydroxysteroid dehydrogenase message and increasing hexose-6-phosphate dehydrogenase message in liver |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
11beta-HSD1 inhibition may be a valid target for the treatment of diabetes |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
11beta-HSD1 is a drug target for treatment of insulin resistance, diabetes and cardiovascular disease |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
inhibiting 11beta-HSD1 activity signifies a promising therapeutic strategy in the treatment of type 2 diabetes and related diseases |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
measures of 11beta-HSD1 enzyme activity can predict the response of bone formation markers to therapeutic glucocorticoids |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
at baseline, mRNA levels are similar in skeletal muscle of diabetic and control sugjects for 11beta-HSD1, 11beta-HSD2, and hexose-6-phosphate dehydrogenase. 11beta-HSD1 activity is reduced in diabetic subjects, while 11beta-HSD2 activity is increased. After application of dexamethasone, 11beta-HSD1 mRNA increases in both groups, whereas 11beta-HSD2 mRNA decreases. 11beta-HSD1 activity increases in diabetic subjects, but not in controls, whereas 11beta-HSD2 activity does not change in either group; mRNA levels are similar in diabetic and control subjects for 11beta-hydroxysteroid dehydrogenase 1 and 11beta-hydroxysteroid dehydrogenase 2. 11beta-Hydroxysteroid dehydrogenase 2-activity is higher in diabetic patients. After treatment with dexamethasone, 11beta-hydroxysteroid dehydrogenase 1-mRNA increases in both groups, whereas 11beta-hydroxysteroid dehydrogenase 2-mRNA decreases. 11beta-Hydroxysteroid dehydrogenase 1-activity increases in diabetic patients, but not in control, whereas 11beta-hydroxysteroid dehydrogenase 2-activity does not change in either group |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
curcumin is inhibitory to isoform 11beta-HSD1 in intact cells with IC50 value of 5.79 microM, competitive. Treatment with curcumin reduces serum glucose, cholesterol, triglyceride, low density lipoprotein levels in high-fat-diet-induced obese rats |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
the enzyme activity is inversely associated with urinary cortisol/cortisone levels and it is not associated with the subclinical hypercortisolism complications |
| 1.1.1.146 | 11beta-hydroxysteroid dehydrogenase |
medicine |
in breast cancer tissue, cholesterol epoxide hydrolase ChEH metabolizes cholesterol-5,6-epoxide into cholestane-3beta,5alpha,6beta-triol, which is transformed into the oncometabolite 6-oxo-cholestan-3beta,5alpha-diol by 11beta-hydroxysteroid-dehydrogenase 11betaHSD2. ChEH inhibition and 11betaHSD2 silencing inhibit 6-oxo-cholestan-3beta,5alpha-diol production and tumor growth. Patient breast cancer samples show significantly increased 6-oxocholestan-3beta,5alpha-diol levels and greater ChEH and 11betaHSD2 protein expression compared with normal tissues, and 11betaHSD2 and ChEH overexpression correlate with a higher risk of patient death |
| 1.1.1.B40 | 11beta-hydroxysteroid dehydrogenase (NAD+) |
medicine |
exposure of fetus to high levels of synthetic glucocorticoid may have long-lasting effects on the hippocampal expression of hypothalamic-pituitary-adrenal-related genes into adulthood |
| 1.1.1.B40 | 11beta-hydroxysteroid dehydrogenase (NAD+) |
medicine |
squirrel monkeys protect the mineralocorticoid receptor from activation by high cortisol levels in the kidney via upregulation of 11beta-HSD2 activity through increased production of the enzyme |
| 1.1.1.B40 | 11beta-hydroxysteroid dehydrogenase (NAD+) |
medicine |
treatment of rats with dehydroepiandrosterone induces a shift from isoform 11beta-HSD1 to 11beta-HSD2 expression, increasing conversion from active to inactive glucocorticoids |
| 1.1.1.B40 | 11beta-hydroxysteroid dehydrogenase (NAD+) |
medicine |
high-fat fed animals overexpress 11beta-hydroxysteroid dehydrogenase type 2 in subcutaneous but not in retroperitoneal fat. Enzyme mRNA levels strongly correlate in both tissues with different parameters related to obesity, such as body weight, adiposity, and insulin resistance |
| 1.1.1.B40 | 11beta-hydroxysteroid dehydrogenase (NAD+) |
medicine |
11beta-HSD1 is a drug target for treatment of insulin resistance, diabetes and cardiovascular disease |
| 1.1.1.B40 | 11beta-hydroxysteroid dehydrogenase (NAD+) |
medicine |
age-related reduced 11beta-HSD2 activity contributes to the rising prevalence of arterial hypertension in elderly |
| 1.1.1.B40 | 11beta-hydroxysteroid dehydrogenase (NAD+) |
medicine |
at baseline, mRNA levels are similar in skeletal muscle of diabetic and control sugjects for 11beta-HSD1, 11beta-HSD2, and hexose-6-phosphate dehydrogenase. 11beta-HSD1 activity is reduced in diabetic subjects, while 11beta-HSD2 activity is increased. After application of dexamethasone, 11beta-HSD1 mRNA increases in both groups, whereas 11beta-HSD2 mRNA decreases. 11beta-HSD1 activity increases in diabetic subjects, but not in controls, whereas 11beta-HSD2 activity does not change in either group; mRNA levels are similar in diabetic and control subjects for 11beta-hydroxysteroid dehydrogenase 1 and 11beta-hydroxysteroid dehydrogenase 2. 11beta-Hydroxysteroid dehydrogenase 2-activity is higher in diabetic patients. After treatment with dexamethasone, 11beta-hydroxysteroid dehydrogenase 1-mRNA increases in both groups, whereas 11beta-hydroxysteroid dehydrogenase 2-mRNA decreases. 11beta-Hydroxysteroid dehydrogenase 1-activity increases in diabetic patients, but not in control, whereas 11beta-hydroxysteroid dehydrogenase 2-activity does not change in either group |
| 1.1.1.141 | 15-hydroxyprostaglandin dehydrogenase (NAD+) |
medicine |
15-hydroxyprostaglandin dehydrogenase hypomorphic mice show a decreased level of enzyme mRNA and activity in all tissues examined. Mice show spontaneous preterm labor in the absence of progesterone withdrawal, and the onset of labor is preceded by prematurely increased concentrations of prostaglandin E2 and F2alpha. The fetal genotype plays a role in birth timing |
| 1.1.1.141 | 15-hydroxyprostaglandin dehydrogenase (NAD+) |
medicine |
A140P is a naturally occuring mutation in patients with pulmonary hypertrophic osteoarthropathy. Homozygous individuals develop pulmonary hypertrophic osteoarthropathy secondary to chronically elevated prostaglandin E2 levels. Heterozygous relatives also show milder biochemical and clinical manifestations. Identification of an insertion-deletion mutation in 15-hydroxyprostaglandin dehydrogenase exon 3, this alters the open reading frame from codon 78, truncating the protein after ten altered amino acids, and of a homozygous 2-bp deletion within the duplicated dinucleotide CTCT at nucleotides 175 and 176. This alters the reading frame from residue 59 and truncates the HPGD protein at residue 65 after seven altered amino acids. Both of these predicted truncated proteins lack the entire PGE2-binding domain and cause primary hypertrophic osteoarthropathy |
| 1.1.1.141 | 15-hydroxyprostaglandin dehydrogenase (NAD+) |
medicine |
expression in nontumorigenic IEC-18 cells, with and without K-RasV12 and analysis of the ability of cells to form tumors in nu/nu mice. Transformed cells show increased 15-hydroxyprostaglandin dehydrogenase activity with decreased prostaglandin E2 and prostaglandin I2 levels, cyclooxygenase-2 and microsomal prostaglandin E synthase-1 expression and proliferation rates. Xenografts of cells expressing both the enzyme and K-RasV12 exhibit delayed tumor formation with negligible cyclooxygenase-2 and microsomal prostaglandin E synthase-1 expression and significantly decreased prostaglandin E2 levels. Tumors have decreased staining of the proliferative marker, Ki-67, and a significant increase in apoptosis in the central region of the tumor |
| 1.1.1.141 | 15-hydroxyprostaglandin dehydrogenase (NAD+) |
medicine |
in non-small-cell lung cancer cells, i.e. NSCLC cells, much lower expression of 15-hydroxyprostaglandin dehydrogenase in all histologic groups compared with healthy lung cell. Treatment with the epidermal growth factor receptor tyrosine kinase inhibitor erlotinib increases the expression of the enzyme in a subset of NSCLC lines |
| 1.1.1.141 | 15-hydroxyprostaglandin dehydrogenase (NAD+) |
medicine |
loss of 15-hydroxyprostaglandin expression in 65% of lung cancers. Enzyme acts as a tumor suppressor in lung cancer and is a direct downstream effector of hepatocyte nuclear factor 3beta |
| 1.1.1.141 | 15-hydroxyprostaglandin dehydrogenase (NAD+) |
medicine |
thiazolidinediones rosiglitazone and pioglitazone upregulate expression of 15-hydroxyprostaglandin dehydrogenase, involving peroxisome proliferator-activated receptor gamma. Upregulation results in reduced production of prostaglandin E2 and finally inhibition of lung cancer growth |
| 1.1.1.141 | 15-hydroxyprostaglandin dehydrogenase (NAD+) |
medicine |
up-regulation of cyclooxygenase-2 expression by pro-inflammatory cytokines is accompanied by down-regluation of 15-hydroxyprostaglandin dehydrogenase expression. Over-expression of cyclooxygenase-2 but not -1 also attenuates 15-hydroxyprostaglandin dehydrogenase expression. Similarly, overexpression of 15-hydroxyprostaglandin dehydrogenase inhibits interleukin 1beta-induced cyclooxygenase-2 expression and results in apoptosis. The levels of 15-hydroxyprostaglandin dehydrogenase expression in transfected cells correlate positively with those of mesenchymal markers, and negatively with those of epithelial markers |
| 1.1.1.141 | 15-hydroxyprostaglandin dehydrogenase (NAD+) |
medicine |
PGDH expression suppresses K-RasV12-mediated tumorigenesis in intestinal epithelial cells |
| 2.1.1.182 | 16S rRNA (adenine1518-N6/adenine1519-N6)-dimethyltransferase |
medicine |
KsgA as a possible anti-microbial drug target |
| 2.1.1.182 | 16S rRNA (adenine1518-N6/adenine1519-N6)-dimethyltransferase |
medicine |
the presence of a functional rRNA dimethylase enzyme belonging to the KsgA family in Chlamydia present an excellent chemotherapeutic target |
| 2.1.1.B123 | 16S rRNA (uridine1369-2'-O)-methyltransferase |
medicine |
mutation G189R identified in a 7-year-old boy with childhood-onset rapidly progressive encephalomyopathy and stroke-like episodes. Multiple OXPHOS defects and decreased mtDNA copy number (40%) are detected in muscle homogenate. Symptoms are similar to mitochondrial encephalopathy, lactic acidosis and stroke-like episodes (MELAS) syndrome. A yeast MRM2 knockout mutant shows a defect in respiration and the reduction of the 2'-O-methylmodification at position U2791 in the yeast mitochondrial 21S rRNA. Complementation of the yeast knockout mutant with the human mutant Mrm2 fails to rescue the respiratory phenotype, which is instead completely rescued by expressing the wild-type allele |
