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Search term: medicine

Results 1 - 100 of 6717 > >>
EC Number
Application
Commentary
alcohol dehydrogenase
medicine
organ simulations indicate that higher therapeutic acetaminophen (0.5 mM) inhibits 16% of allotype ADH1B*1/*1 hepatic ADH activity at 2-20 mM ethanol and that therapeutic salicylate (1.5 mM) inhibits 30-31% of the allotype ADH1B*2/*2 activity, suggesting potential significant inhibitions of ethanol first-pass metabolism in these allelotypes
alcohol dehydrogenase
medicine
isozyme ADH2 is a target for anti-amoebic agents
alcohol dehydrogenase (NADP+)
medicine
drugs for testing function of liver and kidney
alcohol dehydrogenase (NADP+)
medicine
daunorubicin, a cancer chemotherapeutic agent can be reduced by aldehyde reductase
alcohol dehydrogenase (NADP+)
medicine
ability of aldehyde reductase from liver to reduce certain cancer chemotherapeutic antibiotics suggested a role for this enzyme in drug metabolism
alcohol dehydrogenase (NADP+)
medicine
brain aldehyde reductase activity is closely associated with pharmalogical actions of drugs affecting the central nervous system, anti-convulsant drugs have inhibitory effects, more work is needed for the mechanism of action of psychoactive drugs and interactions of barbiturates with aldehyde reductase
alcohol dehydrogenase (NADP+)
medicine
inhibitors alrestatin and sorbinil, possible method of preventing neuropathy and cataractogenesis associated with diabetes
alcohol dehydrogenase (NADP+)
medicine
-
alcohol dehydrogenase (NADP+)
medicine
enzyme as a target for anti-tuberculosis and other drugs
alcohol dehydrogenase (NADP+)
medicine
enzyme as a target for anti-tuberculosis and other drugs; enzyme may be an interesting target for development of new anti-mycobacterial agents
glycerol-3-phosphate dehydrogenase (NAD+)
medicine
the hyperthyroid status leads to a significant decrease and the hypothyroid status to a significant increase of both enzyme amount and activity in both female and male animals. The euthyroid and hyperthyroid females show a higher activity and the hyperthyroid females also show a higher enzyme amount in comparison with male animals, while the hypothyroid animals show low levels in both sexes. The enzyme-dependent oxygen consumption of freshly isolated liver mitochondria from hyperthyroid animals is higher compared with euthyroid animals, and is activated bycoenzyme Q analogue idebenone, in both euthyroid and hyperthyroid rats. Determination of enzyme amount and activity can serve as an additional criterion for the evaluation of the thyroid hormone status
L-iditol 2-dehydrogenase
medicine
target for inhibitor design in hyperglycaemia and diabetes mellitus treatment
L-iditol 2-dehydrogenase
medicine
target for inhibitor design
aldehyde reductase
medicine
enzyme protein levels and activity decrease progressively during heart failure upon rapid left ventricular pacing, such as myocardial capacity to detoxify lipid-peroxidation derived aldehydes
aldehyde reductase
medicine
myocardial enzyme activity is increased during ischemia, partially due to activation by nitric oxide, enzyme inhibition increases glycolysis and glucose oxidation
aldehyde reductase
medicine
inhibition of enzyme by tolrestat or sorbinil prevents apotosis and activation of calpase-3, attenuation of TNF-alpha and hyperglykemia-induced activation of protein kinase C, but does not prevent the activation of transkription factor NK-kappaB and protein kinase C by phorbol ester, enzyme is an obligatory mediator of the apoptotic events upstream of protein kinase C
aldehyde reductase
medicine
pharmacological inhibition of enzyme significantly reduces ischemic injury and improves functional recovery in enzyme transgenic mice
aldehyde reductase
medicine
inhibition of enzyme prevents TNF-alpha-induced increase in Bax and Bak and the downregulation of Bcl-2, inhibition abrogates Ap-1 DNA binding activity and prevents the activation of caspase-3, JNK, and p38 MAPK in cells stimulated by TNFalpha
aldehyde reductase
medicine
inhibition of enzyme inhibits vascular smooth muscle cell growth upon injuries via a decrease in activity of transcription factor NF-kappaB
aldehyde reductase
medicine
inhibition of enzyme by zolrestat attenuates apoptosis in sorbitol-treated cells. Hyperosmolarity-induced cell death requires induction of enzyme as well as a decrease in intracellular glutathione levels
aldehyde reductase
medicine
inhibition of AR may assist in the chemotherapy of malignant tumors by suppressing the rapid growth of cancer cells
aldehyde reductase
medicine
treatment with the nitric oxide synthase inhibitor, N-nitro-L-arginine methyl ester prevented ischemia-induced aldose reductase activation and myocardial sorbitol accumulation in rat hearts subjected to global ischemia ex vivo or coronary ligation in situ, whereas inhibition of inducible nitric oxide synthase and neuronal nitric oxide synthase have no effect. Activation of aldose reductase in the ischemic heart is abolished by pretreatment with peroxynitrite scavengers hesperetin or 5,10,15,20-tetrakis-[4-sulfonatophenyl]-porphyrinato-iron [III]
aldehyde reductase
medicine
inhibition of AR may be a significant therapeutic approach in preventing bacterial endotoxin-induced sepsis and tissue damage
aldehyde reductase
medicine
inhibition/antisense abolition of aldose reductase inhibits the tumor necrosis factor alpha-induced synthesis of prostaglandin E2 and the activity of cyclooxygenase. Inhibition of aldose reductase prevents tumor necrosis factor alpha-induced activation of protein kinase C and NF-kappaB which results in the abrogation of Cox-2 mRNA and protein expression
aldehyde reductase
medicine
in streptozotocin-diabetic mice, aldose reductase inhibitor treatment or genetic deficiency of aldose reductase result in significant dephosphorylation of both peroxisome proliferator-activated receptor alpha and ERK1/2
aldehyde reductase
medicine
inhibition of enzyme in neural stem cells exposed to high glucose concentration results in decrease of oxidative stress, restoration of cell viability and proliferation, and reduction of apoptotic cell death. Inhibition attenuates the down-regulation of glucose transporter 1 expression
aldehyde reductase
medicine
ALR2 is a critical target to prevent and control diabetic complications through the inhibition of its activity
aldehyde reductase
medicine
inhibition of aldose reductase may represent a useful strategy for treating vascular inflammation associated with diabetes
aldehyde reductase
medicine
levels of ALR2 activity as well as sorbitol in erythrocytes may have value as a quantitative trait to establish a risk profile for development of diabetic retinopathy, type 2 diabetic patients with diabetic retinopathy show significantly higher specific activity of ALR2 as compared to type 2 diabetic patients without diabetic retinopathy
aldehyde reductase
medicine
aldose reductase ALR2 is a target enzyme for the treatment of diabetic complications
aldehyde reductase
medicine
the enzyme may be a potential drug target or vaccine candidate for schistosomes
UDP-glucose 6-dehydrogenase
medicine
possibility that gallic acid and quercetin may modulate human breast cancer cell proliferation by inhibiting UGDH
UDP-glucose 6-dehydrogenase
medicine
UGDH content in prostatic acini is a novel candidate biomarker that may complement the development of a multi-biomarker panel for detecting prostate cancer within the tumor adjacent field on a histologically normal biopsy specimen
glyoxylate reductase
medicine
identification of point mutations and minor deletions resulting in primary hyperoxaluria type 2
L-lactate dehydrogenase
medicine
potential drug target for new antimalarials
L-lactate dehydrogenase
medicine
structural characterization of the enzyme and active-site differences from the human lactate dehydrogenase may be useful for structural-based design of new treatments for toxoplasmic infections
L-lactate dehydrogenase
medicine
suitable drug target for design of novel babesial chemotherapeutics
L-lactate dehydrogenase
medicine
serum LDH zymograms of patients can be used as prognostic marker, since they tend to reach the normal level during recovery signifying the effect of chemotherapy in hospitalized patients. Elevation along with the rise in total LDH activity may be used in the diagnosis and monitoring of tubercular pyothorax
L-lactate dehydrogenase
medicine
the enzyme is a target for treatment of cancer
glycerate dehydrogenase
medicine
glyoxylate reductase/hydroxypyruvate reductase is a prognostic marker for hepatocellular carcinoma patients after curative resection
hydroxymethylglutaryl-CoA reductase (NADPH)
medicine
the enzyme is a target for intervention in the treatment of hypercholesterolaemia, clinical utility of inhibitors to decrease the levels of atherogenic lipiproteins in patients
hydroxymethylglutaryl-CoA reductase (NADPH)
medicine
dual therapy with the HMG-CoA reductase inhibitor pravastatin and the angiotensin receptor antagonist olmesartan, which produce an additive reduction in cardiomyocyte hypertrophy and cardiac fibrosis after myocardial infarction through different mechanisms, decreases the propensity of the heart to arrhythmogenesis
hydroxymethylglutaryl-CoA reductase (NADPH)
medicine
genistein, eicosapentaenoic acid and docosahexaenoic acid down-regulate reductase activity, primarily through posttranscriptional effects. Diets rich in soy isoflavones and fish oils, therefore, may exert anti-cancer effects through the inhibition of mevalonate synthesis in the breast. Genistein and docosahexaenoic acid, in particular, may augment the efficacy of statins, increasing the potential for use of these drugs in adjuvant therapy for breast cancer
hydroxymethylglutaryl-CoA reductase (NADPH)
medicine
the cholesterol absorption inhibitor ezetimibe profoundly lowers serum cholesterol levels in animals expressing very low rates of hepatic cholesterol synthesis and produces large compensatory increases in hepatic HMG-CoA reductase expression without signifucantly affecting expression of hepatic low density lipoprotein receptors. This indicates that ezitimibe should be most effective in lowering serum cholesterol levels in peaple with low rates of cholesterol synthesis/High rates of cholesterol absorption
hydroxymethylglutaryl-CoA reductase (NADPH)
medicine
treatment with the inhibitor atorvastatin exerts early nephroprotective effects in a rat model of chronic inhibition of nitric axide synthesis
3-hydroxyacyl-CoA dehydrogenase
medicine
lack of Hadh2 activity may impart early developmental problems, leading to embryo lethality. In addition to the 3-hydroxyacyl-CoA dehydrogenase activity, the HSD10 (formerly Hadh2) activity is also relevant to the metabolism and meiotic maturation of oocytes
3-hydroxyacyl-CoA dehydrogenase
medicine
HADH protects against excess amino acid-induced insulin secretion
malate dehydrogenase
medicine
therapy development for sexually transmitted disease of humans
malate dehydrogenase (decarboxylating)
medicine
ME2 as a potentially novel metabolic target for leukemia therapy
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
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
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
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
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
11beta-hydroxysteroid dehydrogenase (NAD+)
medicine
age-related reduced 11beta-HSD2 activity contributes to the rising prevalence of arterial hypertension in elderly
11beta-hydroxysteroid dehydrogenase (NAD+)
medicine
11beta-HSD1 is a drug target for treatment of insulin resistance, diabetes and cardiovascular disease
isocitrate dehydrogenase (NADP+)
medicine
sensitizing effect of NADP+-dependent isocitrate dehydrogenase siRNA on the apoptotic cell death of HeLa cells offers the possibility of developing a modifier of cancer therapy
isocitrate dehydrogenase (NADP+)
medicine
the sensitizing effect of NADP+-dependent isocitrate dehydrogenase siRNA on the apoptotic cell death of HeLa cells offers the possibility of developing a modifier of cancer chemotherapy
isocitrate dehydrogenase (NADP+)
medicine
transfection of HeLa cells with an NADP+-dependent isocitrate dehydrogenase small interfering RNA decreased the activity of IDPm, enhancing the susceptibility of radiation-induced apoptosis. The effect of NADP+-dependent isocitrate dehydrogenaseIDPm small interfering RNA on HeLa cells offers the possibility of developing a modifier of radiation therapy
phosphogluconate dehydrogenase (NADP+-dependent, decarboxylating)
medicine
with a deficiency of 6-phosphogluconate dehydrogenase some reticulocytosis occurs
phosphogluconate dehydrogenase (NADP+-dependent, decarboxylating)
medicine
-
phosphogluconate dehydrogenase (NADP+-dependent, decarboxylating)
medicine
6PGDH might be a target for chemotherapy against parasitic infections as trypanosomiasis
phosphogluconate dehydrogenase (NADP+-dependent, decarboxylating)
medicine
6-phosphogluconate dehydrogenase is a potential target for new drugs against African trypanosomiasis
L-gulonate 3-dehydrogenase
medicine
role in an alternative pathway of the production of xylitol in the lens that causes cataracts in mammalian organisms
glucose-6-phosphate dehydrogenase (NADP+)
medicine
refolding protocol can be applied to produce high recovery yield of folded protein with unaltered properties, paving the way for future studies on clinical G6PD mutants with folding defects and providing a useful model system to study the folding process of oligomeric proteins
glucose-6-phosphate dehydrogenase (NADP+)
medicine
G6PD deficiency due to its polymorphism causes neonatal jaundice, acute hemolysis in malaria, favism, severe chronic non-spherocytic hemolytic anemia, and lipid dysregulation. G6PD deficiency may be responsible for the high incidence of coronary artery disease among African-Americans and reduces mortality due to ischemic heart disease and cerebrovascular disease in Sardinian males. In Mediterranean and Sardinian G6PD-deficient individuals, G6PD deficiency may confer a partial protection against atherosclerosis, leading to a reduced risk of cardiovascular diseases in G6PD-deficient individuals. G6PD appears to be an attractive therapeutic target for diabetes-induced cardiomyopathy, ischemic cardiomyopathy, pulmonary hypertension, angiotensin II-induced hypertension, vascular smooth muscle hypertrophy and coronary disease in humans
glucose-6-phosphate dehydrogenase (NADP+)
medicine
G6PD deficiency is the commonest clinically significant enzymopathy in humans. More than 400 million people worldwide are affected by this condition which may determine favism, drug-induced acute hemolytic anemia, severe chronic nonspherocytic haemolytic anemia, neonatal jaundice and hemolytic anemia associated with viral or microbiological infections. The highest prevalence of G6PD deficiency mainly regards tropical Africa, the Middle East, tropical and subtropical Asia, Papua New Guinea, and various Mediterranean regions, for example Sardinia island. G6PD deficiency may represent a selective advantage due to the increased resistance to severe Plasmodium falciparum infection of the affected individuals. G6PD/pyruvate kinase ratio is more reliable than the G6PD activity alone, for the identification of G6PD heterozygotes, especially in patients with microcytic anemia. G6PD/6PDG ratio is an absolute measure of G6PD deficiency of female carriers
glucose-6-phosphate dehydrogenase (NADP+)
medicine
in Vietnam the blackwater fever syndrome is associated with malaria infection, quinine ingestion and G6PD deficiency. G6PD deficiency is a major risk factor for haemoglobinuria in ethnic Vietnamese Kinh and within the G6PD deficient population G6PD Viangchan is significantly associated with haemoglobinuria
glucose-6-phosphate dehydrogenase (NADP+)
medicine
fluoride-containing bioactive glasses as used in tissue engineering as well as bone repair, inhibit the pentose phosphate oxidative pathway and the glucose 6-phosphate dehydrogenase activity. The effects are ascribable to the fluoride content/release of glass powders, they are mimicked by NaF solutions and are prevented by radical scavengers dimethyl sulfoxide and tempol, by superoxide dismutase, and by glutathione, but not by apocynin
3alpha-hydroxysteroid 3-dehydrogenase (Si-specific)
medicine
enzyme as part of commercial enzyme test kit for bile acid content in serum as an index for hepatic diseases
3alpha-hydroxysteroid 3-dehydrogenase (Si-specific)
medicine
enzyme is a potential drug target
3(or 17)beta-hydroxysteroid dehydrogenase
medicine
inhibitor Strogen forte extract can be used for treatment of benign prostatic hyperplasia
17beta-estradiol 17-dehydrogenase
medicine
binding of equilin at the active site of the enzyme is the basis for inhibition of reduction of estrone to estradiol. One possible outcome of estrogen replacement therapy in vivo can be the reduction of estradiol levels in breast tissues and hence the reduced risk of estrogen-dependent breast cancer
17beta-estradiol 17-dehydrogenase
medicine
attractive drug target in hormone-sensitive breast cancer
17beta-estradiol 17-dehydrogenase
medicine
target for suppression of estrogen synthesis in breast cancer
17beta-estradiol 17-dehydrogenase
medicine
as estradiol stimulates the growth and development of hormone-dependent breast cancer, inhibition of the final step of its synthesis is an attractive target for the treatment of this disease
17beta-estradiol 17-dehydrogenase
medicine
estrogenic response for estrone is enhanced by the local action of HSD17B1 in vivo. Thus the enzyme is a potential target for pharmacological inhibition of estrogen activation. Targeted inhibition of HSD17B1 is a promising therapeutic approach to modulate estrogen response in the target tissue with less severe side effects as compared with antiestrogens
17beta-estradiol 17-dehydrogenase
medicine
type 1 17beta-hydroxysteroid dehydrogenase is an interesting biological target for designing drugs for the treatment of estrogen-sensitive diseases such as breast cancer
17beta-estradiol 17-dehydrogenase
medicine
inhibitors of the enzyme have potential as treatments for hormone dependent breast cancer; inhibitors of the enzyme have potential as treatments for hormone dependent breast cancer
17beta-estradiol 17-dehydrogenase
medicine
17beta-HSD1 is an attractive target for the treatment of mammary tumours; 17beta-HSD1 is an attractive target for the treatment of mammary tumours
17beta-estradiol 17-dehydrogenase
medicine
17beta-HSD1 inhibitors such as STX1040 may provide a treatment for hormone-dependent breast cancer
17beta-estradiol 17-dehydrogenase
medicine
17beta-HSD1 is overexpressed in many breast tumors. Thus, it is an attractive target for the treatment of these diseases
17beta-estradiol 17-dehydrogenase
medicine
disease iondications for HSD17B1 inhibitors in disorders in the female reproductive organs associated with enhanced androgen action, such as ovarian serous cystadenomas
17beta-estradiol 17-dehydrogenase
medicine
application of medroxyprogestrone acetate, dydrogesterone and dienogest significantly decreases isoforms HSD17B1 and CYP19A1 expression and significantly increases isoform HSD17B2 expression. Dydrogesterone and dienogest also significantly suppress estrogen receptors ESR1 and ESR2 transcription, whereas medroxyprogestrone acetate and dydrogesterone significantly reduce mRNA levels of G protein-coupled estrogen receptor 1. Results thus suggest that in peritoneal endometriosis the beneficial effects of these progestins can be explained by lower HSD17B1 and higher HSD17B2 mRNA and protein levels, which lead to reduced local estradiol biosynthesis; application of medroxyprogestrone acetate, dydrogesterone and dienogest significantly decreases isoforms HSD17B1 and CYP19A1 expression and significantly increases isoform HSD17B2 expression. Dydrogesterone and dienogest also significantly suppress estrogen receptors ESR1 and ESR2 transcription, whereas medroxyprogestrone acetate and dydrogesterone significantly reduce mRNA levels of G protein-coupled estrogen receptor 1. Results thus suggest that in peritoneal endometriosis the beneficial effects of these progestins can be explained by lower HSD17B1 and higher HSD17B2 mRNA and protein levels, which lead to reduced local estradiol biosynthesis
17beta-estradiol 17-dehydrogenase
medicine
17beta-hydroxysteroid dehydrogenase type 2 is mainly involved in the conversion of estradiol into estrone. Their ratio is decreased from 9/1 to 7/3 after over-expression of 17beta-hydroxysteroid dehydrogenase type 2 in MCF-7 cells already over-expressing 17beta-hydroxysteroid dehydrogenase type 1. The ratio is further decreased by the addition of the oxidative cofactor, NAD, to the cell culture to facilitate the estradiol to estrone conversion catalyzed by 17beta-hydroxysteroid dehydrogenase type 2; twenty four hours after addition of different concentrations of estrone and estradiol, the ratio stabilizes to around 9/1 in breast cancer cell lines with high expression of 17beta-hydroxysteroid dehydrogenase type 1, such as T47D, BT 20, and JEG 3 cells, whereas it approaches 1/5 in cells with low expression of 17beta-hydroxysteroid dehydrogenase type 1, such as MCF-7 cells. The estradiol/estrone concentration ratio is modified to 9/1 in MCF-7 and HEK-293 cells over-expressing 17beta-hydroxysteroid dehydrogenase type 1. In T47D and BT 20 cells , this ratio is decreased from 9/1 to nearly 1/5 after 17beta-hydroxysteroid dehydrogenase type 1 knockdown by specific siRNAs
17beta-estradiol 17-dehydrogenase
medicine
Patients with oestrogen positive tumours with high isoform 17betaHSD14 expression have fewer local recurrences when treated with tamoxifen compared to patients with lower tumoural 17betaHSD14 expression, for whom tamoxifen does not reduce the number of local recurrences. No prognostic importance of 17betaHSD14 is seen for systemically untreated patients
17beta-estradiol 17-dehydrogenase
medicine
isoform 17betaHSD6 is expressed in estrogen receptor beta-positive epithelial cells of the human prostate. In prostate cancers of Gleason grade higher than 3, both estrogen receptor beta and isoform 17betaHSD6 are undetectable
testosterone 17beta-dehydrogenase (NADP+)
medicine
exposure of HCT-15 cells to cisplatin results in aquisition of cisplatin resistance and concomitant induction of isoform AKR1C3 and aldo-keto reductase AKR1C1 expression. The resistance lowers the sensitivity toward cellular damages evoked by oxidative stress-derived aldehydes, 4-hydroxy-2-nonenal and 4-oxo-2-nonenal that are detoxified by AKR1C1 and AKR1C3. Overexpression of AKR1C1 or AKR1C3 in the parental HCT15 cells mitigates the cytotoxicity of the aldehydes and cisplatin. Knockdown of both AKR1C1 and AKR1C3 in the resistant cells or treatment of the cells with specific inhibitors of the aldo-keto reductases increases the sensitivity to ciplatin toxicity. Pretreatment of the resistant cells with proteasome inhibitor Z-Leu-Leu-Leu-al augments the cisplatin sensitization elicited by aldo-keto reductase inhibitors
testosterone 17beta-dehydrogenase (NADP+)
medicine
uniform, diffuse, and strong expression of isoform AKR1C3 in normal endometrial epithelium but not in endometrial stromal cells. The expression of AKR1C3 is reduced in both hyperplastic and carcinomatous endometrial epithelium
testosterone 17beta-dehydrogenase (NADP+)
medicine
positive isoform AKR1C3 immunoreactivity is extensively present in both adenocarcinoma and squamous cell carcinoma arising from the lung and the gastroesophageal junction. Isoform AKR1C3 immunoreactivity is absent in small cell carcinoma of the lung
homoisocitrate dehydrogenase
medicine
detection of unique gene LYS1 for rapid identification of pathogenic fungi, LYS1 gene is a possible target for selective inhibition of growth of pathogenic fungi in vivo
hydroxymethylglutaryl-CoA reductase
medicine
target enzyme for chemotherapy of hypercholesterolemias
hydroxymethylglutaryl-CoA reductase
medicine
pterygium has an altered metabolism of cholesterol, namely increased LDL-R and HMG-CoA-R mRNAs. Both genes may play important roles in the pathogenesis of pterygium
hydroxymethylglutaryl-CoA reductase
medicine
in endotoxemic mice, leukocyte infiltration in the liver is significantly elevated. Simvastatin significantly reduces endotoxin-induced hepatocellular damage and apoptosis. Hepatic accumulation of leukocytes is attenuated by simvastatin. Co-administration of mevalonate abolishes the protective effects of simvastatin on endotoxin-provoked increases in serum alanine transferase and serum alanine transferase as well as leukocyte recruitment
all-trans-retinol dehydrogenase (NAD+)
medicine
mutations in RDH12 are associated with Leber congenital amaurosis
GDP-6-deoxy-D-talose 4-dehydrogenase
medicine
L122C and R130C are missence mutations found in patients with inborn error of isoleucine degradation, almost complete loss of enzyme activity
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
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
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; PGDH expression suppresses K-RasV12-mediated tumorigenesis in intestinal epithelial cells
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
Results 1 - 100 of 6717 > >>