Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A mycobacterial expression-secretion vector was constructed in which the Escherichia coli alkaline phosphatase (phoA) reporter gene was placed under the control of the Mycobacterium tuberculosis 85A promoter and secretion signal sequences. In recombinant Mycobacterium smegmatis and Mycobacterium bovis BCG, PhoA activity could readily be detected on the mycobacterial cell surface and in the culture supernatant, indicating that the 85A signals can drive heterologous expression and secretion in both species. In contrast to the mycobacteria, the 85A promoter did not function in E. coli. We mapped the promoter region by progressive deletions using BAL 31 exonuclease and by primer extension analysis. Insertion and deletion mutations within the promoter region indicated that, unlike most E. coli promoters but similar to Streptomyces promoters, the position of the putative -35 region was not critical for efficient promoter activity. In addition, we investigated the ability of the identified signals to drive the production and secretion in BCG of recombinant Schistosoma mansoni glutathione S-transferase (Sm28GST), a protective antigen against schistosomiasis. BALB/c mice immunized with the recombinant BCG by a single dose exhibited a weak but specific T-cell response to Sm28GST.
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PMID:Analysis of the Mycobacterium tuberculosis 85A antigen promoter region. 783 98

Resistance of tumor cells to doxorubicin is a multifactorial phenomenon. In the present investigation, the ability of resistance modifiers against different resistance mechanisms was analysed. Substances which block P-glycoprotein (P-170) function circumvented resistance of doxorubicin-resistant sarcoma 180 (S180) cells completely (verapamil, thioridazine) or partially (hycanthone), whereas inhibitors of glutathione S-transferase (ethacrynic acid, N-ethylmaleimide, buthionine sulfoximine), and protein kinase C (staurosporine, acridine orange) caused only a partial reversion of resistance. In contrast, an inhibitor of alkaline phosphatase (levamisole) did not overcome doxorubicin-resistance. These results indicate that P-glycoprotein blockers might be more effective to modulate doxorubicin-resistance of S180 cells as compared to other modifiers. Further investigations using other MDR cell lines are required to clarify the generality of these findings.
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PMID:Reversal of doxorubicin-resistance in sarcoma 180 tumor cells by inhibition of different resistance mechanisms. 810 93

Specific [32P]ADP-ribosylation by Clostridium botulinum exoenzyme C3 was used to study the involvement of phosphorylation in the regulation of the low-molecular-mass GTP-binding protein Rho. Dephosphorylation of CHO cell extracts by alkaline phosphatase treatment resulted in a 80-90% reduction in the C3-catalysed [32P]ADP-ribosylation of Rho proteins in both cytosolic and membrane fractions. Similar results were obtained after dephosphorylation with protein phosphatase type-1 from bovine retina, whereas type-2B and type-2C phosphatases had no effect on the level of subsequent [32P]ADP-ribosylation of Rho by C3. Incubation of CHO cell lysate under phosphorylation conditions increased the subsequent C3-mediated [32P]ADP-ribosylation of Rho proteins. The protein kinase inhibitors H7 and H9 had no effect on [32P]ADP-ribosylation at concentrations which are specific for inhibition of protein kinase A or C. Recombinant glutathione S-transferase-RhoA fusion protein (GST-RhoA) was phosphorylated by protein kinase A; however, the phosphorylation had no stimulatory effect on the ADP-ribosylation of GST-RhoA by C3. An approx. 48 kDa phosphoprotein was identified which bound specifically to recombinant GST-RhoA fusion protein. By gel-permeation chromatography, Rho-containing complexes of approx. 50 kDa and 130-170 kDa were detected. The ADP-ribosylation of Rho in the 130-170 kDa complex was reduced by alkaline phosphatase pretreatment. The data suggest that Rho activity is influenced by phosphorylation of Rho-associated regulatory factors. Phosphorylation/dephosphorylation of these Rho-regulating factors appears to alter the ability of Rho to serve as a substrate for C3-induced [32P]ADP-ribosylation.
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PMID:ADP-ribosylation of Rho proteins by Clostridium botulinum exoenzyme C3 is influenced by phosphorylation of Rho-associated factors. 819 24

In an animal model of hormone-mediated carcinogenesis, male golden Syrian hamsters develop renal carcinoma following prolonged exposure to 17beta-estradiol. The basis for the species and tissue specificity is unclear. Detailed information on the disposition of 17beta-estradiol in this model is lacking. Because catechol estrogens have been implicated in this model of carcinogenesis, we investigated the metabolism and nephrotoxicity of 17beta-estradiol in golden Syrian hamsters, with emphasis on the formation of catechol estrogen thioethers. 17beta-Estradiol (50 micromol/kg, i.p.) is a mild nephrotoxicant, causing significant elevations in the urinary excretion of gamma-glutamyl transpeptidase (gamma-GT), alkaline phosphatase, glutathione S-transferase (GST) and glucose. Increases in renal protein carbonyls and lipid hydroperoxides, which are markers of oxidative damage, also occur after administration of 17beta-estradiol (50 micromol/kg, i.p.). 17beta-Estradiol-mediated nephrotoxicity is reduced by treating animals with acivicin, an inhibitor of gamma-GT, implying that toxicity is mediated by metabolites requiring metabolism by this enzyme. Following administration of 17beta-[14C]estradiol (100 micromol/kg) to hamsters, 9.7% of the dose is recovered in bile after 5 h, the majority (7.9%) representing aqueous metabolites. Seven catechol estrogen GSH conjugates were identified, 2-hydroxy-1,4-bis-(glutathion-S-yl)-17beta-estradiol, 2-hydroxy-4-(glutathion-S-yl)-17beta-estradiol, 2-hydroxy-4-(glutathion-S-yl)-estrone, 4-hydroxy-1-(glutathion-S-yl)-estrone, 2-hydroxy-1-(glutathion-S-yl)-estrone, 4-hydroxy-1-(glutathion-S-yl)-17beta-estradiol, and 2-hydroxy-1-(glutathion-S-yl)-17beta-estradiol. At 5.4 micromol/kg of 17beta-estradiol, a dose-reflective of daily exposure levels in the hamster model of nephrocarcinogenicity, 12% of the dose is recovered within 5 h as a combination of GSH conjugates of 2- and 4-hydroxy-17beta-estradiol and 2- and 4-hydroxyestrone. In summary, oxidation of catechol estrogens, followed by GSH conjugation, occurs in vivo and 17beta-estradiol is a mild nephrotoxicant in a manner dependent on the activity of gamma-GT.
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PMID:Formation of catechol estrogen glutathione conjugates and gamma-glutamyl transpeptidase-dependent nephrotoxicity of 17beta-estradiol in the golden Syrian hamster. 906 57

1. alpha-Tocopherol (alpha-T) and gamma-tocotrienol (gamma-T) were supplemented continuously for 8 weeks in the diets of normal rats and rats chemically induced with cancer using diethylnitrosamine (DEN), 2-acetylaminofluorene (AAF) and partial hepatectomy. Hepatocarcinogenesis was followed by determining the plasma gamma-glutamyl-transpeptidase (GGT) and alkaline phosphatase (ALP) activities as well as placental glutathione S-transferase (PGST) and GGT activities histochemically, at 4-week intervals. 2. Male Rattus norvegicus were supplemented alpha-T and gamma-T at two different doses of 30 and 300 mg/kg diet. The supplementation was started at three different times: simultaneously with DEN administration; 4 weeks; and 8 weeks after DEN administration. 3. Elevation of plasma GGT activities and formation of PGST and GGT positive foci were attenuated significantly (P < 0.05) when alpha-T and gamma-T were supplemented simultaneously with cancer induction. Supplementation begun 4 and 8 weeks after cancer induction did not affect plasma enzyme activities and formation of enzyme-positive foci. 4. alpha-T was more effective than gamma-T, and a lower dose of 30 mg/kg was found to be more effective in reducing the severity of hepatocarcinogenesis.
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PMID:Different starting times of alpha-tocopherol and gamma-tocotrienol supplementation and tumor marker enzyme activities in the rat chemically induced with cancer. 914 29

Dietary zinc deficiency in rats causes increased osmotic fragility of their erythrocytes. In this study, the influence of supplementary antioxidants (vitamin C, vitamin E or beta-carotene) on osmotic fragility, oxidative damage and components of the primary defense system of erythrocytes of zinc-deficient rats was investigated. Indicators of hemolysis in vivo were also examined. Five groups of 12 male rats were force-fed a zinc-adequate diet (control rats), a zinc-deficient diet or a zinc-deficient diet enriched with vitamin C, vitamin E or beta-carotene. Compared with the control rats, the rats fed the zinc-deficient diet without supplementary antioxidants had greater red blood cell osmotic fragility, higher concentrations of thiobarbituric acid-reactive substances and alanine, higher glutathione S-transferase activity, lower concentration of glutathione and activity of glutathione peroxidase as well as lower activity of superoxide dismutase in plasma (P < 0.05). Supplementation with antioxidants generally improved osmotic fragility in zinc-deficient rats without influencing zinc concentration or alkaline phosphatase activity in plasma, indicators of zinc status. At some of the hypotonic saline concentrations tested, vitamin C and beta-carotene significantly affected osmotic fragility. The zinc-deficient rats fed a diet without supplementary antioxidants had significantly higher concentrations of alanine in erythrocytes than the zinc-deficient rats supplemented with vitamin C, vitamin E or beta-carotene and had significantly higher levels of thiobarbituric acid-reactive substances in erythrocytes than the rats supplemented with beta-carotene. There was no indication of hemolysis in vivo in rats fed zinc-deficient diets. The results show that supplementary antioxidants decrease osmotic fragility and oxidative damage of erythrocytes in zinc-deficient rats.
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PMID:Supplementation with vitamin C, vitamin E or beta-carotene influences osmotic fragility and oxidative damage of erythrocytes of zinc-deficient rats. 920 82

The present study was designed to investigate the effect of antioxidant supplementation on the in vitro osmotic fragility of erythrocytes from zinc-deficient rats. Rats were fed either a zinc-adequate diet, zinc-deficient diet or a zinc-deficient diet enriched either with vitamin C or vitamin E or beta-carotene. Components of the primary antioxidant system of erythrocytes, parameters of hemolysis in vivo and indicators of liver injuries were also examined. In order to ensure adequate and identical food intake rats were force-fed by intragastric tube. The supplementation with antioxidants led to a marked improvement of the osmotic fragility without having influenced zinc status of the animals and components of the antioxidant system. The strongest effect was exerted by vitamin E. The rats fed the zinc-adequate diet (control group) showed unusually high values of erythrocytes osmotic fragility. Therefore there was no difference between control group and zinc-deficient group. A possible reason for this is discussed. Zinc deficiency led to a reduction of serum zinc concentration and alkaline phosphatase activity as well as to changes in the antioxidant system of erythrocytes characterized by a decrease of glutathione and an increase of glutathione S-transferase activity. Superoxide dismutase activity in serum decreased. There was no indication for hemolysis in vivo and for liver injuries.
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PMID:Influence of vitamin C, vitamin E and beta-carotene on the osmotic fragility and the primary antioxidant system of erythrocytes in zinc-deficient rats. 927 23

The 14-3-3 protein family has been implicated in growth factor signaling. We investigated whether 14-3-3 protein is involved in insulin signaling in 3T3L1 adipocytes. A significant amount of insulin receptor substrate 1 (IRS-1) was immunodetected in the immunoprecipitate with anti-14-3-3beta antibody at the basal condition. 100 nM insulin increased the amount of IRS-1 in the immunoprecipitate 2.5-fold. The effect of insulin was abolished by 100 nM wortmannin. An in vitro binding study revealed that glutathione S-transferase-14-3-3beta fusion protein directly associates with recombinant IRS-1. Pretreatment of recombinant IRS-1 with alkaline phosphatase clearly decreased this association. Because the recombinant IRS-1 was not phosphorylated on its tyrosine residues, the results suggest that serine/threonine phosphorylation of IRS-1 is responsible for the association. When the cells are treated with insulin, phosphatidylinositol 3'-kinase (PI3K) is supposed to complex either 14-3-3beta-IRS-1 or IRS-1. The 14-3-3beta-IRS-1-PI3K and IRS-1-PI3K complexes were separately prepared by a sequential immunoprecipitation, first with anti-14-3-3beta and then with anti-IRS-1 antibodies. The specific activity of the PI3K in the former was approximately half of that in the latter, suggesting that 14-3-3beta protein bound to IRS-1 inhibits insulin-stimulated lipid kinase activity of PI3K in 3T3L1 adipocytes.
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PMID:14-3-3beta protein associates with insulin receptor substrate 1 and decreases insulin-stimulated phosphatidylinositol 3'-kinase activity in 3T3L1 adipocytes. 942 53

The subchronic toxicity of antimony in drinking water was studied in the rat. Male and female Sprague-Dawley rats (127-135 g body weight, 15 animals per group) were exposed to a soluble trivalent antimony salt, potassium antimony tartrate, in drinking water at concentrations of 0.5, 5, 50 and 500 ppm for 13 wk. Control rats received tap water as drinking water. An additional 10 male and 10 female rats were included in each of the control and 500 ppm groups and were given tap water for a further 4-wk recovery period after the 13-week treatment period. During treatment, the highest dose animals of both sexes consumed significantly less water and showed suppressed body weight gain. During recovery, water intake was quickly restored to that of the control groups and body weight gain was accelerated. At termination, one highest dose male had a cirrhotic liver, and three highest dose males exhibited gross haematuria. Female rats showed a dose-related decrease in serum glucose starting at 5 ppm, and rats of both sexes in the highest dose group had slightly decreased alkaline phosphatase activity and creatinine. The highest dose males had decreased red blood cell and platelet counts and increased mean corpuscular volume. Hepatic glutathione S-transferase activity was increased in the highest dose males and females and ethoxyresorufin-O-deethylase activity was increased in the highest dose males. In the highest dose groups, mild adaptive histological changes were observed in the thyroid, liver and pituitary gland of both sexes, and in the spleen of male rats and thymus of female rats. After a 4-wk recovery period, the pituitary gland of both sexes appeared normal and the changes in the liver and thyroid of both sexes became less severe. On the other hand, minimal changes persisted in the spleen of both sexes and in the thymus of males. Tissue antimony levels were dose-related and follow the order: red blood cells > > spleen, liver > kidney > brain, fat > serum. After the recovery period, antimony level in the highest dose animals decreased for all tissues except the spleen, which remained the same as before recovery. A NOAEL of 0.5 ppm antimony in drinking water, equivalent to an average intake of 0.06 mg/kg body weight/day, was established on the basis of the histological and biochemical changes observed at 5.0 ppm.
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PMID:Effects of antimony on rats following 90-day exposure via drinking water. 948 61

Cadmium induced lipid peroxidation (LPO) and the activity of antioxidant enzymes after the administration of a single dose of CdCl2 (0.4 mg kg-1 body wt, i.p.) was studied in rat erythrocytes. Cd intoxication increased erythrocyte LPO along with a decrease in superoxide dismutase (SOD) up to three days of Cd treatment. The decrease in erythrocyte catalase (CAT) activity was marked within 9 h of Cd intoxication. After three days of Cd treatment, LPO decreased towards normal, along with an increase in erythrocyte SOC and CAT activity. Blood glutathione (GSH) decreased significantly within 24 h of Cd treatment, followed by an increase towards normal. Erythrocyte glutathione S-transferase (GST) activity increased up to 10 days of Cd intoxication, probably in an attempt to reduce Cd toxicity. Serum glutamate pyruvate transaminase (SGPT), serum alkaline phosphatase (SALP) and serum bilirubin increased up to 10 days of Cd intoxication. Blood urea increased significantly up to three days, followed by a decrease towards normal. The results show that Cd induced LPO was associated with a decrease in antioxidant enzymes and GSH in erythrocytes; as these antioxidants increase in erythrocytes with recovery from Cd intoxication, the Cd induced LPO reversed towards normal. The increase in the SGPT, SALP and serum bilirubin correlated with LPO. The results suggest that Cd intoxication induces oxidative stress and alters the antioxidant system, resulting in oxidative damage to rat erythrocytes.
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PMID:Lipid peroxidative damage on cadmium exposure and alterations in antioxidant system in rat erythrocytes: a study with relation to time. 954 68


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