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)

In a mating mixture of Hfr and F- bacteria the gene for alkaline phosphatase undergoes a transient derepression at the time of transfer. It is shown that this escape from repression occurs in the donor cells and is probably connected with the synchronous duplication of the transferred genome.
Mol Gen Genet 1980
PMID:Depression of alkaline phosphatase in Hfr of Escherichia coli during conjugation. 700 13

The synthesis of alkaline phosphatase by two strains of Vibrio cholerae belonging to the Inaba and Ogawa serotypes has been examined in relation to the phosphate concentration of the culture medium. The synthesis of the enzyme in both strains was repressed in cells grown in the presence of a high concentration of inorganic phosphate. Lowering the phosphate content of the growth medium led to a derepression of enzyme activity. The presence of glucose in low phosphate medium stimulated the degree of derepression. The synthesis of the enzyme by strain Inaba 569B was more sensitive to inorganic phosphate than that of strain Ogawa 154. The enzyme was presumably located in the periplasmic space since it was released when the organisms were converted to spheroplasts.
J Gen Microbiol 1982 Feb
PMID:Repression of the alkaline phosphatase of Vibrio cholerae. 707 94

This five-year study of 108 patients with giant cell arteritis and/or polymyalgia rheumatica drawn from all departments of a district general hospital emphasizes the difficulties of diagnosis. A correct diagnosis was made by the referring doctor in 33 per cent of patients and on initial attendance at hospital in 67 per cent of patients. Symptoms were present for more than three months before referral to hospital in 39 per cent of patients, and the delay before diagnosis at hospital was greater than one month in 20 per cent. Systemic illness (present in 83 per cent of cases), anaemia (33 per cent), elevated alkaline phosphatase (73 per cent) and raised immunoglobulin levels (48 per cent) caused diagnostic problems in 28 patients at primary care level and in 23 patients at hospital.
J R Coll Gen Pract 1981 May
PMID:Polymyalgia rheumatica and giant cell arteritis--a difficult diagnosis. 731 Jul 59

Growth hormone receptor (GH-R) gene expression was evaluated in avian growth-plate cartilage by Northern blot and hybridization using the avian GH-R probe. A single transcript of approximately 5.2 kb was demonstrated in cultured growth-plate chondrocytes as well as in growth-plate extracts. GH receptor gene expression was inhibited by chicken GH (cGH) in a dose- and time-dependent manner. Chicken GH was more potent in down-regulating the GH-R gene expression than hGH, but on the other hand cGH exhibited a lower affinity to avian chondrocytes receptor than did the human hormone. Addition of ascorbic acid to the culture media caused cell differentiation: induction of alkaline phosphatase activity and attenuation of collagen type II gene expression. No differences in the GH-R gene expression were observed in the nondifferentiated cells compared with the differentiated cells. Chicken GH did not form any complex with the purified hGH binding protein (hGHBP), did not bind to human lymphocytes GH receptor, and did not affect Nb2 cell proliferation. These systems represent somatogenic and lactogenic types of GH receptors, respectively. In summary, avian growth-plate chondrocytes in situ and in culture exhibit GH-R and these receptors are capable of binding GH. Thus, the failure of GH to affect avian chondrocytes' proliferation was not due to either the absence of receptors on the cell membrane or to a lack in its binding activity, but rather may be due to events farther downstream.
Gen Comp Endocrinol 1993 Nov
PMID:Growth hormone receptors in avian epiphyseal growth-plate chondrocytes. 750 82

A ribozyme was constructed of the catalytic domain of tobacco ringspot virus satellite RNA and flanking sequences complementary to the target, secreted alkaline phosphatase (SEAP) mRNA. The ribozyme specifically cleaved the substrate in vitro; compared with that constant temperature. The relationship between specific endoribonuclease activity of the ribozyme and Mg2+ concentration was shown. The ribozyme was active in 293 cell line which was cotransfected with plasmids carrying the SEAP gene under control of RSV LTR promoter and the ribozyme gene under early HCMV promoter: SEAP activity reduced by half.
Mol Gen Mikrobiol Virusol
PMID:[In vitro and in vivo study of the activity of secreted alkaline phosphatase mRNA ribozyme gene]. 773 97

The mechanism of G protein-mediated inhibition of an inwardly rectifying K+ current (IIR) in adrenal chromaffin cells was investigated using the whole-cell version of the patch clamp technique. In case of recording with use of ATP-containing patch solution, the IIR was well maintained; otherwise, it ran down within 15 min. This run down was not prevented by replacement with adenylyl-imidodiphosphate, a nonhydrolysable analogue of ATP, but was markedly reduced by the addition to the ATP-free solution of 1 microM calyculin A, a specific inhibitor of serine/threonine phosphatase 1 (PP1) and 2A (PP2A). The addition of alkaline phosphatase to the ATP-containing solution facilitated run down of the current, and application of 100 microM H-7, a general kinase inhibitor, reversibly suppressed IIR. These results taken together suggest that inwardly rectifying K+ channels are under the influence of kinase and phosphatase without external signals. Infusion of nonhydrolysable analogues of GTP, guanosine-5'-O-(3-thiophosphate) (GTP gamma S) or guanylyl-imidodiphosphate, through the pipette produced little inward current at -55 mV, but completely inhibited IIR within approximately 5 or 6 min in all cells tested in the presence of 12 microM Mg2+ inside the cell. In contrast, infusion of aluminum fluoride (AlF) complex, another GTP binding (G) protein activator, consistently produced large inward currents, but did not alter IIR noticeably for 15 min in 17% of the cells tested. In the other cells, the inhibition of IIR developed slowly after long latent periods. This inhibitory potency of AlF was not enhanced by an increase in Mg2+ concentrations. Subtraction of the current-voltage relationship before from that noted during the generation of inward current by AlF complex revealed that the inward current diminished progressively with hyperpolarizations, as is the case with a nonselective cation current (INS) induced by a muscarinic agonist. Thus, AlF complex seems to be potent with the generation of INS, but not with IIR inhibition. The addition of 3 microM calyculin A significantly retarded the IIR inhibition by GTP gamma S, whereas that of 1 microM okadaic acid, another inhibitor of PPI and PP2A, markedly prevented the decline of IIR by AIF complex. Our observations suggest that the low potency of AlF complex in inhibiting IIR may be due to interference with phosphatase activity and that the activation of G protein suppresses IIR, probably by enhancing the apparent activity of phosphatase, which may explain run down of the current.
J Gen Physiol 1995 Feb
PMID:Phosphatase is responsible for run down, and probably G protein-mediated inhibition of inwardly rectifying K+ currents in guinea pig chromaffin cells. 776 18

A putative movement protein of molecular mass 50 kDa encoded by the ORF2 of the apple chlorotic leaf spot virus (ACLSV) genome was expressed in Escherichia coli using an expression vector and was then used to produce an antiserum. Immunoblot analysis using an antiserum raised against this protein showed that the ORF2 protein of ACLSV was detected in both cell wall and cell membrane fractions prepared from infected Chenopodium quinoa tissues. The ORF2 protein from infected tissues had a molecular mass of 52 kDa, larger than that of the full-length ORF2 protein (50 kDa protein) expressed in E. coli. Incubation of the 52 kDa protein with alkaline phosphatase resulted in a decrease in its apparent molecular mass from 52 kDa to 50 kDa, strongly suggesting that the ORF2 protein of ACLSV is phosphorylated in infected plant tissues.
J Gen Virol 1995 Jun
PMID:Expression, subcellular location and modification of the 50 kDa protein encoded by ORF2 of the apple chlorotic leaf spot trichovirus genome. 778 79

1. The hepatoprotective activity of aqueous-methanolic extract of Cyperus scariosus (Cyperaceae) was investigated against acetaminophen and CCl4-induced hepatic damage. 2. Acetaminophen produced 100% mortality at a dose of 1 g/kg in mice while pretreatment of animals with plant extract (500 mg/kg) reduced the death rate to 30%. 3. Acetaminophen at a dose of 640 mg/kg produced liver damage in rats as manifested by the rise in serum levels of alkaline phosphatase (ALP), glutamate oxaloacetate transaminase (GOT) and glutamate pyruvate transaminase (GPT) to 430 +/- 68, 867 +/- 305 and 732 +/- 212 IU/l (n = 10) respectively, compared to respective control values of 202 +/- 36, 59 +/- 14 and 38 +/- 7. 4. Pretreatment of rats with plant extract (500 mg/kg) significantly lowered (P < 0.05) the respective serum ALP; GOT and GPT levels to 192 +/- 31, 63 +/- 9 and 35 +/- 8. 5. The hepatotoxic dose of CCl4 (1.5 ml/kg; orally) raised serum ALP, GOT and GPT levels to 328 +/- 30, 493 +/- 102 and 357 +/- 109 IU/l (n = 10) respectively, compared to respective control values of 177 +/- 21, 106 +/- 15 and 47 +/- 12. 6. The same dose of plant extract (500 mg/kg) was able to significantly prevent (P < 0.05) CCl4-induced rise in serum enzymes and the estimated values of ALP, GOT and GPT were 220 +/- 30, 207 +/- 95 and 75 +/- 38, respectively. 7. The plant extract also prevented CCl4-induced prolongation in pentobarbital sleeping time confirming hepatoprotectivity.(ABSTRACT TRUNCATED AT 250 WORDS)
Gen Pharmacol 1995 May
PMID:Studies on protective effect of Cyperus scariosus extract on acetaminophen and CCl4-induced hepatotoxicity. 778 38

The present work was carried out to study the involvement of lipid peroxidation in immobilization-induced damage of the rat lung. Thirty-hour immobilization stress was found to result in a marked morphological alteration of the lung ultrastructure and in significant increases of both acid and alkaline phosphatase for immobilization times exceeding 12 and 24 hours respectively. Also, increased concentrations of conjugated dienes and fluorescent products of lipid peroxidation were measured in the lungs of rats immobilized over 12 h. Immobilization stress was followed by significant changes in the fatty acid contents of lung phospholipids. The levels of polyunsaturated fatty acids C-18:2 (linoleic acid) and C-20:4 (arachidonic acid) were decreased even during the alarm phase. The contents of monounsaturated fatty acids did not change, while those of saturated fatty acids slightly increased. The involvement of lipid peroxidation in immobilization-induced damage of the rat lung was indirectly supported by the observation of decreased levels of vitamin E at 12 h immobilization. All the above data suggest that lipid peroxidation is somehow involved in the immobilization-induced damage of the rat lung. The observed changes in lipid peroxidation preceded the immobilization stress-induced damage of the lung cell membranes. Therefore, it seems likely that lipid peroxidation is the cause, rather than a consequence of the stress-altered lung structure.
Gen Physiol Biophys 1994 Dec
PMID:Immobilization stress enhances lipid peroxidation in the rat lungs. Materials and methods. 779 54

The phoE promoter region in Escherichia coli contains a -10 region, typical of sigma 70-dependent promoters and, instead of a normal -35 region, a so-called pho box, to which the transcriptional activator phospho-PhoB binds under low phosphate conditions. A second pho box is present upstream of the first one and is required for full expression of phoE during phosphate starvation. To determine whether the lack of expression under high phosphate conditions is due solely to the absence of a genuine -35 box, the -10 region was further optimized towards the consensus -10 sequence and promoter activity was measured using alkaline phosphatase as a reporter. The mutations resulted in a drastic increment in the basal level of expression under high phosphate conditions, indicating that the deviations from consensus in the -10 region also play a role in determining the poor expression of the wild-type promoter under these conditions. The expression under high phosphate conditions was partly dependent on the presence of the phoB gene, showing that a small amount of active PhoB must be present under these circumstances. During phosphate starvation, the activity of the mutant promoters was further induced. The upstream pho box was not required for full expression from the mutant promoters under these conditions. Apparently, the wild-type phoE promoter is carefully balanced by deviations from the optimal Pribnow box sequence that reduce expression under high phosphate conditions and by the presence of several copies of the pho box, which enhance expression under phosphate starvation.
Mol Gen Genet 1994 Oct 28
PMID:Effect of mutations in the -10 region of the phoE promoter in Escherichia coli on regulation of gene expression. 781 30


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