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)

The activity of the enzyme ornithine decarboxylase (ODC) is increased in confluent culture of two breast cancer cell lines (T47D and MCF-7) following a change of medium. The increase in activity is maximum at 12 hours and this level is reduced in cells treated with high concentrations of HuIFN-alpha. However, the increased level of ODC activity seen in the first few hours after medium change can be stimulated by low concentrations of interferon (10-100 units per ml). The activity of the acidic and alkaline phosphatase of the above cell lines are affected by HuIFN-alpha similar to ODC. In stimulating levels of ODC and phosphatases, interferon is acting similar to mitogens, and in T47D and MCF-7 cells this stimulatory effect precedes the inhibitory effect more commonly seen in interferon-treated cells.
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PMID:Ornithine decarboxylase and phosphatase activity can be stimulated by low concentrations of interferon in human breast cancer cell lines. 285 Oct 88

Aluminum (Al) accumulation in bone is associated with low bone formation and mineralization rates; resorption may also be reduced. The mechanism of these Al-induced changes was investigated using cultured mouse osteoblast-like (OB) and osteoclast-like (OC) cells. The Al effect on bone resorption was measured by the in vitro release of 45Ca and beta-glucuronidase from mouse fetal limb-bones. Al had a biphasic effect. High concentrations (greater than 1.5 X 10(-6) M) of Al inhibited collagen and DNA synthesis, ornithine decarboxylase and alkaline phosphatase activity in OB, and depressed tartrate-resistant acid phosphatase activity in OC. Lower Al concentrations stimulated these cellular activities and 45Ca and beta-glucuronidase release from fetal bones. Al had no effect on basal cAMP levels in OB but inhibited the stimulating effect of bPTH on cAMP content. Al also altered the 1,25(OH)2D3 effects on the ornithine decarboxylase activity of OB cells. These data suggest that: (i) the low bone formation observed in vivo during Al intoxication may be due to the inhibition of collagen synthesis and to depressed cell proliferation; and (ii) Al may indirectly influence bone remodeling by interfering with the actions of bPTH and 1,25(OH)2D3 on bone cells.
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PMID:Aluminum action on mouse bone cell metabolism and response to PTH and 1,25(OH)2D3. 303 86

Ornithine decarboxylase (ODC) of Tetrahymena pyriformis is inactivated by E. coli or calf intestinal alkaline phosphatase. Inactivated ODC by E. coli alkaline phosphatase, form b, can be allosterically reactivated to form a by purine-nucleosides or -nucleotides at 10(-4) M concentration. Inactivated ODC by calf intestinal alkaline phosphatase bound to agarose can be converted to form a by purine-analogues with 10(-7) M concentration only if inorganic phosphate is included in the incubation mixture. Pyridoxal phosphate, phosphoamino acids or other phospho-compounds are incapable to promote the conversion of b form to a form of ODC. These data suggest that purine-analogues may be the in vivo physiological regulators of ODC of T. pyriformis.
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PMID:Allosteric activation by purine nucleosides and nucleotides of the inactive by phosphatase ornithine decarboxylase of Tetrahymena pyriformis. 313 58

To evaluate the roles of ornithine decarboxylase (ODC) and polyamines in the regulation of epithelial repair, rabbit mid-small intestine after transient ischaemic villus injury in the presence and absence of DL-difluoromethylornithine (DFMO), an irreversible inhibitor of ODC was studied. Rabbits received 2% (w/v) DFMO in drinking water for two days before undergoing a sham laparotomy, or a 90 minute mesenteric vascular occlusion of 20 cm of mid-intestine. DFMO fed and control rabbits were studied four, 24, 72, or 120 hours after this ischaemic intestinal injury. In controls, ischaemic injury caused shortened villi at four hours (p less than 0.01), diminished mucosal sucrase and alkaline phosphatase activities at 24 hours (p less than 0.05), but raised ODC (p less than 0.001) and thymidine kinase (p less than 0.01) activities at four hours with recovery by 72 hours. DFMO treatment significantly reduced ODC activity at all stages of the experiment and significantly inhibited the rise in activity observed after injury (p less than 0.01). Mucosal concentrations of the polyamines, spermidine and spermine, were similar in the sham operated groups; four hours and 24 hours after ischaemia, they increased in the DFMO animals (p less than 0.01) but fell (p less than 0.05) in those that did not receive DFMO. After ischaemic injury, DFMO treatment inhibited ODC but failed to influence recovery of villus structure or enzyme activities in the small intestine. We conclude that ODC and the polyamines, spermidine and spermine, are not key regulators of small intestinal repair after transient ischaemia.
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PMID:Failure of ornithine decarboxylase inhibition to alter small intestinal epithelial repair after transient segmental ischaemia. 313 52

Two major ionic forms of ornithine decarboxylase were separated by column chromatography of extracts of kidneys from androgen-treated male CD-1 mice on DEAE-Sepharose CL-6B, and purified individually to apparent homogeneity. On SDS-PAGE, a single major protein band of Mr 50000 was present in each. When incubated with casein kinase II, purified from rat liver cytosol, only one form of the enzyme, which represented 20% of the total ornithine decarboxylase in the tissue, became phosphorylated. The major form, which was eluted later from the column, could be phosphorylated only after treatment with alkaline phosphatase, indicating that the phosphatase removed enzyme-bound phosphate already attached at the casein kinase II phosphorylation site. Evidence for the occurrence of a phosphorylated form of the enzyme in kidneys of dexamethasone-treated rats is also presented.
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PMID:Multiple ionic forms of ornithine decarboxylase differ in degree of phosphorylation. 316 22

Estradiol (E2) stimulates the proliferation of human endometrial adenocarcinoma cells of the Ishikawa line, which had been previously shown to respond to estrogen by increasing their levels of progesterone receptor and the specific activities of DNA polymerase alpha and alkaline phosphatase. Although E2 (10(-8) M) did not increase rates of proliferation during the initial logarithmic growth period of the cultures under the chosen experimental conditions (MEM with 15% charcoal-treated fetal bovine serum renewed every 2-3 days), it sustained cell proliferation after about day 10, when parallel control cultures had reached plateau cell densities. Cell proliferation in control cultures at plateau levels was resumed when the hormone was added. Growth rates of cultures containing E2 from the time of seeding and the proportion of quiescent cells, estimated by using a simple cell kinetic model, decreased steadily with time. Ornithine decarboxylase and DNA polymerase alpha activities, as well as estrogen receptor levels, also decreased with time in culture. Ishikawa cells formed colonies in soft agar; colony formation efficiencies were higher as the number of cells seeded was increased from 10,000 to 100,000 cells/6 cm dish, were not influenced by the addition of E2 to the medium (10(-9) to 10(-5) M) and were markedly reduced by difluoromethylornithine (10(-2) M), an effect that was counteracted by putrescine (25 X 10(-6) M).
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PMID:Effects of estradiol on proliferation of endometrial adenocarcinoma cells (Ishikawa line). 380 63

The antilymphocytic and antiphlogistic agent cyclosporin A (CsA) inhibits in vivo various effects induced by the tumor promoting phorbol ester 12-0-tetradecanoylphorbol-13-acetate (TPA). These include the edema of the mouse ear, the alkaline phosphatase (AP) activity and the ornithine decarboxylase (ODC) activity in mouse epidermis as well as the generation of a specific arachidonic acid (AA) metabolite in mouse epidermis. AA metabolism in an epidermal cell-free system of mouse epidermis was not suppressed by CsA. According to thin layer chromatography the TPA-induced and as yet unidentified AA metabolite exhibits a polarity between that of 5-HETE and 12-/15-HETE. Studies with inhibitors indicate it to be a lipoxygenase product.
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PMID:Cyclosporin A inhibits biological effects of tumor promoting phorbol esters. 391 31

In adult sparse-fur mutant mice, ornithine transcarbamylase (OTC) activity represents only 14% of the normal values. We studied the development of this activity from birth to adult period and demonstrated that the enzyme deficiency is already fully expressed at birth, in both the liver and the small intestine of mutants. Since OTC catalyzes the conversion of ornithine to citrulline, in the presence of carbamoyl-phosphate, the effect of a disturbed ornithine metabolism on the postnatal development of the small intestine has been evaluated. The normal appearance of sucrase as well as the normal increase of glucoamylase, trehalase, and alkaline phosphatase activities are delayed in sparse-fur mice compared with controls. Moreover, normal adult values are never attained. In contrast, the normal decline of lactase activity is impaired while leucylnaphthylamidase activity is unaffected. Cell proliferation, as evaluated by [3H]thymidine incorporation into DNA and mitotic index, is less active during the 3rd wk of life in mutants. These phenomena are closely associated with a transient weak arginase and ornithine decarboxylase activity in the small intestine. Since arginase catalyzes the conversion of arginine to orthithine, thus ensuring the availability of this substrate for ornithine decarboxylase activity, these results indicate a disturbance of polyamine metabolism in mutant enterocytes with a consequent delay in postnatal differentiation and proliferation. Sparse-fur mutant mouse may therefore represent a useful animal model for evaluating the role of ornithine metabolism in the maturation process of the small intestine.
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PMID:Postnatal maturation of enterocytes in sparse-fur mutant mice. 395 97

Folded periosteal explants derived from 16-day-old chick embryo calvariae differentiate and form bone when cultured for 6 days in chemically defined, hormone-supplemented medium or on plasma clots. We studied the effect of dexamethasone on generation of cells with osteoblastic phenotype in such cultures. Bone cell phenotype was evaluated by determination of alkaline phosphatase (AP) activity. Cellular proliferation was assessed by measuring ornithine decarboxylase (ODC) activity, [3H]thymidine uptake, and radioautography of cultures that had incorporated [3H]thymidine. Cultures were exposed to various medium concentrations of dexamethasone (10(-6) M, 10(-7) M, 10(-8) M) from the outset or from the second or fourth day of culture onwards. In cultures continuously exposed to dexamethasone and maintained in chemically defined media or on plasma clots, dexamethasone increased AP activity measured at day 6. This effect was maximal at 10(-7) M dexamethasone. Cultures exposed to dexamethasone after day 2 in culture also showed increased AP activity, but only in the cultures maintained on plasma clots. There was no stimulation of AP activity when dexamethasone was added at day 4 of culture with either medium, thus suggesting that the effect of glucocorticoids depends on the stage of differentiation of the cultures. In addition to AP stimulation, dexamethasone also stimulated ODC activity. Since ODC activity has been associated with mesenchymal cell proliferation, this suggested that dexamethasone stimulated the proliferation of similar cells in the cultured periostea. Measuring [3H]thymidine uptake in and performing autoradiography of control cultures and cultures treated with dexamethasone confirmed that stimulation of proliferation did occur and located this proliferation within the cell layer adjacent to the bone surface. These results demonstrate that dexamethasone stimulates in vitro osteogenesis, and that this effect appears to be mediated through stimulation of progenitor cell proliferation. In addition, our data indicate that factors in the clot medium modulate the responsiveness of the precursor cell population.
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PMID:Dexamethasone stimulates osteogenesis in chick periosteum in vitro. 404 82

The influence of somatostatin on discrete stages of collagenous-matrix-induced endochondral bone formation has been investigated. Local injection of somatostatin, i.e., without any measurable systemic effect, resulted in a 75% reduction of cell proliferation as measured by [3H]thymidine incorporation and ornithine decarboxylase activities. The minimum effective inhibitory dose of somatostatin was 0.25 microgram/day. Twice daily local injections of the hormone during cartilage formation also resulted in an inhibition, but this was shown to be due to impaired cell proliferation rather than to a direct effect of somatostatin on differentiation. Injection of somatostatin into developing bone tissue after the cartilage stage impaired osteogenesis, assessed by 45Ca incorporation and alkaline phosphatase activity. Concurrent injections of insulin and somatostatin obliterated the inhibitory effect of the latter on cell proliferation. Somatostatin can locally regulate the proliferation and differentiation of chondroprogenitor and osteoprogenitor cells in vivo and may directly contribute to the regulation of bone growth by its ability to counteract the stimulatory effect of insulin.
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PMID:Somatostatin can locally inhibit proliferation and differentiation of cartilage and bone precursor cells. 611 56


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