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)

The immune response to Vibrio cholerae was studied in baboons, rhesus monkeys and marmosets inoculated by the oral, intraintestinal or intravenous route with various strains of V. cholerae. Sera were collected from all animals on days 2, 6, 10, 17, 24, 32, 45 and 60 after infection. Serum protein, immunoglobulins (IgA, IgG, IgM), GOT, and alkaline phosphatases were determined. The results showed that baboons and rhesus monkeys were not susceptible to cholera infection under these experimental conditions. However, we were able to induce a lethal cholera infection in cotton-topped marmosets. In baboons and rhesus monkeys serum IgG levels decreased significantly following inoculation with V. cholerae; however, the ratio of GOT, alkaline phosphatase and antibodies against toxin were only slightly modified.
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PMID:[Experimental cholera in monkeys]. 10 13

Cholera enterotoxin, 45 mug per 250 g body weight, administered intravenously to rats, caused a 6-fold rise in the activity of liver alkaline phosphatase in 12 hr. There was no change in bile volume or in the concentration or total bile content of Na+, K+, HCO3-, or Cl- for 36 hr after the administration of cholera toxin. However, bile phospholipid output fell markedly from a control level of 15.0 +/- 1.0 mumol per 6 hr to a low level of 4.0 +/- 1.2 mumol per 6 hr in the 12- to 18-hr collection, P less than 0.001. There was a similar fall in bile acid secretion, from a control value of 9.8 +/- 0.4 mumol per 6 hr to 4.1 +/- 0.9 mumol in the 12- to 18-hr period, P less than 0.01. The cholera effect was prolonged. Bile acid and phospholipid secretion rates did not return to control values until 30 to 36 hr after the administration of cholera enterotoxin. The cholera toxin-induced reductions in bile acid and phospholipid secretion into bile did not appear to be mediated by adenyl cyclase or cyclic AMP because neither glucagon, a known stimulator of liver adenyl cyclase, nor dibutyryl cyclic AMP had any effect on the secretion into bile of bile acids or phospholipid. The administration of cholera toxin was not associated with any increase in the secretion of free choline into bile. Glucagon and dibutyryl cyclic AMP, two other substances known to increase the activity of rat liver alkaline phosphatase, also had no stimulatory effect on the secretion of free choline into bile. The results do not support the hypothesis that the main function of rat liver alkaline phosphatase is to facilitate the excretion of free choline into bile.
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PMID:Effects of cholera enterotoxin, glucagon, and dibutyryl cyclic AMP on rat liver alkaline phosphatase, bile flow, and bile composition. 17 82

The serum alkaline phosphatase was fractionated by polyacrylamide gel electrophoresis in 317 patients with elevated serum alkaline phosphatase activity. In 253 patients the source of the elevation was the isoenzyme of presumed liver origin, band L. In 87 of these patients, there was either no obvious liver disease or the alkaline phosphatase elevation was inappropriately high. In 19 of the 87, liver disease was further excluded by liver biopsy or by laparotomy. Because of this, biochemical studies were done to verify the hepatic origin of band L. Band L and alkaline phosphatase extracted from human liver migrated together on polyacrylamide gel electrophoresis before and after digestion with Vibrio cholerae neuraminidase. They had identical pH optima, sedimentation coefficients, Michaelis constants, and rates of inactivation at 55.5 degrees C. They had different rates of inactivation in 3 M urea. Over-all, the data indicate that band L is of liver origin, and that elevation of the hepatic alkaline phosphatase isoenzyme may be a nonspecific finding in certain patients.
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PMID:Significance of elevated liver alkaline phosphatase in serum. 109 21

Transforming growth factor-beta (TGF beta) produced by osteoblasts is present in high levels in bone and influences bone formation, replication of bone cells, and expression of osteoblast protein products. Interactions between bone active hormones and locally released and activated TGF beta were studied by examining the influence of TGF beta preincubation on PTH, calcitonin (CT), and vitamin D receptors in an osteoblastic cell line (UMR 106-06). Preincubation of UMR 106-06 cells with 1 ng/ml TGF beta for 3 days increased specific binding of [125I]PTH-related protein (PTHrP)(1-84) to 140% of that in control cells, but [125I]salmon CT binding decreased to 50% of controls. Binding isotherms indicated that the changes in binding were due to altered receptor numbers since affinities for 125I-labeled PTH and CT remained unchanged. The effect on receptor levels was time dependent, requiring 24 h preincubation with TGF beta for measurable changes, and dose dependent, with maximal effects seen with 1 ng/ml TGF beta. Binding of [3H]1,25(OH)2 vitamin D3 was increased to 130% of control in cytosolic extracts of UMR 106-06 cells pretreated for 3 days with 1 ng/ml TGF beta. Scatchard plots suggested an increase in receptor number without change in affinity. The adenylate cyclase response to PTH increased to 150% of control cells after 3 days of treatment with 1 ng/ml TGF beta; however, the adenylate cyclase response to CT was little changed. Forskolin- and cholera toxin-stimulated adenylate cyclase responses were increased by TGF beta treatment to 130-160% of control, indicating an increase in the stimulatory subunit of the G protein. Increased abundance of both Gs and Gi proteins were indicated by increased cholera toxin- or pertussis toxin-dependent [32P] NAD ribosylation of 47-kilodalton (kDa) and 42-kDa or 40-kDa proteins, respectively, in TGF beta-treated cells. Our data support a complex regulatory effect of TGF beta on UMR 106-06 cells with increases in PTH receptors, vitamin D receptors, and G proteins, whereas there is an apparent down-regulation of CT receptors. TGF beta might induce a more differentiated osteoblast phenotype of these cells, which already express differentiated features such as high alkaline phosphatase activity, PTH and vitamin D receptors, and collagenase production. Since low doses of PTH stimulate bone formation in vivo, TGF beta released or activated at sites of new bone formation might locally modulate PTH activity be allowing increased PTH receptor and postreceptor effectiveness.
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PMID:Transforming growth factor-beta modulates receptor binding of calciotropic hormones and G protein-mediated adenylate cyclase responses in osteoblast-like cells. 132 61

Cholera enterotoxin (CT) is produced by Vibrio cholerae and excreted into the culture medium as an extracellular protein. CT consists of one A polypeptide and five B polypeptides associated by noncovalent bonds, and CT-B interacts with CT-A primarily via the A2 domain. Treatment of CT with trypsin cleaves CT-A into A1 and A2 fragments that are linked by a disulfide bond. CT-B binds to ganglioside GM1, which functions as the plasma membrane receptor for CT, and the enzymatic activity of A1 causes the toxic effects of CT on target cells. We constructed translational fusions that joined foreign proteins via their carboxyl termini to the A2 domain of CT-A, and we studied the interactions of the fusion proteins with CT-B. The A2 domain was necessary and sufficient to enable bacterial alkaline phosphatase (BAP), maltose-binding protein (MBP) or beta-lactamase (BLA) to associate with CT-B to form stable, immunoreactive, holotoxin-like chimeras. Each holotoxin-like chimera was able to bind to ganglioside GM1. Holotoxin-like chimeras containing the BAP-A2 and BLA-A2 fusion proteins had BAP activity and BLA activity, respectively. We constructed BAP-A2 mutants with altered carboxyl-terminal sequences and tested their ability to assemble into holotoxin-like chimeras. Although the carboxyl-terminal QDEL sequence of the BAP-A2 fusion protein was not required for interaction with CT-B, most BAP-A2 mutants with altered carboxyl termini did not form holotoxin-like chimeras. When holotoxin-like chimeras containing BAP-A2, MBP-A2, or BLA-A2 were synthesized in V. cholerae, they were found predominantly in the periplasm. The toxin secretory apparatus of V. cholerae was not able, therefore, to translocate these holotoxin-like chimeras across the outer membrane.
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PMID:Fusion proteins containing the A2 domain of cholera toxin assemble with B polypeptides of cholera toxin to form immunoreactive and functional holotoxin-like chimeras. 809 81

An alkaline phosphatase-labeled oligonucleotide DNA probe (CTAP) that was specific for the cholera toxin gene (ctxA) was identified. All cholera toxin-producing strains of Vibrio cholerae, regardless of serotype, hybridized with the CTAP probe, while nontoxigenic strains from either environmental sources or from deletion or substitution mutations did not hybridize. Unlike the whole-gene probes for either ctxA or for the heat-labile toxin or Escherichia coli (eltA), this 23-base sequence did not hybridize with E. coli or with vibrios other than V. cholerae that produce related toxins. By using CTAP to identify colonies grown on nonselective medium, V. cholerae was enumerated at concentrations of 10(3) to 10(7)/g from stool samples of volunteers who had ingested V. cholerae O1 strain 569B. CTAP provides a specific and sensitive tool for diagnosis and environmental monitoring of cholera toxin-producing V. cholerae.
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PMID:Development and testing of a nonradioactive DNA oligonucleotide probe that is specific for Vibrio cholerae cholera toxin. 140 Sep 94

We adapted the electrophoretic method of bone alkaline phosphatase (ALP) determination using neuraminidase from Vibrio cholerae to separate bone and liver ALP on cellulose acetate membrane. Treatment of separator plus serum (1:8, neuraminidase 111 U/l in final) for 10 min at room temperature (25 +/- 1 degree C) and subsequent electrophoresis made it possible to quantify bone ALP activity simply and rapidly. The precision of the data was at the level of CV of 1.6% (within-day) and 4.7% (day-to-day), with recovery rates of 97-103%. The normal range of bone ALP activity depended on age and sex. Seventy-eight diabetes mellitus (DM) patients, excluding those with renal failure, were divided into two groups of those with and without osteopenia with matching of age (+/- 3 years) and sex. Bone ALP (P < 0.001) and total ALP (P < 0.05) activities and urine calcium/creatinine ratio (P < 0.05) were significantly higher in DM with osteopenia than in DM without osteopenia. Therefore, bone formation and absorption may be accelerated in DM with osteopenia in comparison with DM without osteopenia.
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PMID:Cellulose acetate electrophoretic determination of bone alkaline phosphatase activity in healthy subjects and diabetic patients with and without osteopenia. 142 53

When rat endometrial stromal cells from uteri sensitized for decidualization are cultured in vitro, there is an increase in alkaline phosphatase (ALP) activity paralleling that seen in vivo during decidualization. The addition of indomethacin to the culture medium decreases the endogenous production of prostaglandin E2 (PGE2) to below detectable levels and substantially reduces the increase in ALP activity. The addition of either PGE2 or its analog 16,16-dimethyl-PGE2, but not PGF2 alpha or its analog 15(S),15-methyl-PGF2 alpha, overrides this inhibitory effect, suggesting that PGE2 has a specific stimulatory effect upon ALP activity. This in vitro system was used to investigate the role of the cAMP pathway in mediating the stimulatory effect of PGE2 on ALP activity. The data indicate that PGE2 causes an increase in cAMP accumulation by the cells and that the addition of an analog of cAMP or substances which increase the level of cAMP in the cells (1-methyl-3-isobutyl xanthine, cholera toxin, forskolin) causes an increase in ALP activity. Collectively, the results suggest that the stimulatory effect of PGE2 is at least partially mediated by the cAMP pathway.
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PMID:Role of cyclic adenosine 3',5'-monophosphate in mediating the effect of prostaglandin E2 on decidualization in vitro. 171 93

Enzymatic profiles were determined by the API ZYM system for 15 strains of non 01 Vibrio cholerae, 4 strains of V. metschnikovii, 9 strains of V. anguillarum, 6 strains of Plesiomonas shigelloides and 115 strains motile Aeromonas sp. All of the tested strains produced alkaline phosphatase, leucine aminopeptidase and did not possess alpha-fucosidase and alpha-mannosidase. Some differences in enzymatic activities among the tested Vibrionaceae strains were noted. The strains of non 01 V. cholerae, V. metschnikovii, V. anguillarum and P. shigelloides did not produce trypsin, whereas all of the tested Vibrio sp. strains appeared to be positive for this enzyme. Only the strains of P. shigelloides produced BI-Phospho-hydrolase. The lack of acid phosphatase activity was observed among the strains of V. anguillarum.
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PMID:Enzymatic characterization of Vibrionaceae strains isolated from environment and cold-blooded animals. 172 94

An enzyme-based double monoclonal field diagnostic system detecting both serotypes of Vibrio cholerae has been developed. The system uses nitrocellulose as a solid support, 1.25% skimmed dried milk as blocking reagent, water as washing reagent, and alkaline phosphatase cross-linked to antibody by means of glutaraldehyde as detecting reagent. The sensitivity of the system was 10(5) vibrios/ml. The biotin-avidin system gave sensitivity an order of magnitude weaker. There were no cross-reactions with the range of other bacteria tested.
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PMID:The construction of a monoclonal diagnostic system for the field detection of Vibrio cholerae. 190 63


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