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)

Low concentrations of retinol (10 nM-10 microM) and dexamethasone (0.1 nM-1.0 microM) elevated activity of alkaline phosphatase (E.C. 3.1.3.1) in bovine endothelial cells in culture. The effect was apparent after 48 hr of growth in the presence of either of the two compounds, prior to any growth stimulatory effects. A synergistic stimulation of alkaline phosphatase was achieved in the presence of both retinol and dexamethasone implying different mechanisms of induction. Retinoic acid and retinyl acetate also elevated alkaline phosphatase but the retinol analogue reduced in the side chain (perhydroretinol) was inactive. The ability of steroids to elevate alkaline phosphatase activity was associated with the structure commonly required for glucocorticoid activity; however, competitors for the steroid receptor binding failed to prevent the elevation by dexamethasone or the synergism in the presence of retinol and dexamethasone.
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PMID:Synergistic stimulation of alkaline phosphatase activity in bovine aortic endothelial cells grown in the presence of retinoids and glucocorticoids. 404 48

We examined whether chemical agents reported to induce differentiation of leukemic cells also have differentiating effects on normal human granulocytes using alkaline phosphatase activity as a marker. Among 11 compounds examined, only vitamin A analogues were shown to induce this activity in granulocytes from bone marrow of normal individuals. Retinoic acid was the most potent inducer of the activity followed by retinal, whereas retinol and retinol acetate did not induce any activity. The effect on the alkaline phosphatase activity by retinoic acid and retinal was considered to reflect their effect on normal granulocytic differentiation and maturation.
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PMID:Induction of alkaline phosphatase in neutrophilic granulocytes, a marker of cell maturity, from bone marrow of normal individuals by retinoic acid. 405 84

Results of the isotretinoin (13-cis-retinoic acid, Ro 4-3780) German Cooperative Study Group, with 198 acne conglobata patients being treated in 19 departments are reported. For the first 12 weeks (phase I) there was an open assignment to 0.2, 0.5 or 1.0 mg/kilogram bodyweight (kg bw). This was followed by further 12 weeks (phase II). If there was at least a two-third improvement of lesions, the 0.2 mg/kg bw was continued, and the 0.5 mg/kg bw dose lowered to 0.2 mg/kg bw. If there was no such improvement, the dose was elevated to 0.5 and 1.0 mg/kg bw respectively. The initial high dose group of 1.0 mg/kg bw was divided after twelve weeks into 0.2 mg/kg bw maintenance therapy, or no therapy at all. Non-inflammatory and inflammatory acne lesions from the entire body were counted. Seborrhea was graded on a four scale (0 to 3+). Subjective side effects were registered. Laboratory data included hematological profile with differential counts, creatinin, SGOT, SGPT, alkaline phosphatase, total bilirubin, serum cholesterol and serum triglycerides, and urine analysis. For statistical analysis 171 patients were available, 27 dropped out of the study, mostly for reasons unrelated to the drug. At least 75 per cent improvement was seen, in the 0.2 mg/kg bw group in 73.7 and 59.5 per cent respectively; in the 0.5 mg/kg bw group in 72.5 and 61.2 per cent respectively; and in the 1.0 mg/kg bw group in 85.4 and 92 per cent respectively (phase I t12 and phase II t24 values, respectively). Sebum suppression was dose-related. Subjective side effects were fairly well dose-related, particularly those of skin and mucous membranes. Myalgia was rare. There was a dose-related elevation of triglycerides and cholesterol, but not significant for the means of each group. Single patients did show significant elevation of blood lipids. All other laboratory parameters did not change significantly. Isotretinoin is presently the most effective drug to control severe forms of acne, leading to long lasting remissions.
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PMID:[Oral treatment of acne conglobata using 13-cis-retinoic acid. Results of the German multicentric study following 24 weeks of treatment]. 622 51

Cells derived from the G-subline of the Dunning R-3327 rat prostatic adenocarcinoma were selected on the basis of their inducibility for alkaline phosphatase (AP) activity by retinoic acid. A p-nitrophenylphosphate-agarose overlay procedure was used to identify AP-inducible clones. The frequency of AP-inducible cells in one rapidly growing tumorigenic clone, designated 9-1C, has remained at 100% during at least 4 months of continuous culture. In culture, 9-1C cells had a mean population-doubling time in log phase of 14 hr. Retinoic acid (10 microM) did not significantly affect the rate of growth in log phase. It did, however, cause the cultures to saturate at a cell density which was 40% lower than that of control cultures. This effect on saturation density was reversible within 24 hr after removing retinoic acid from the medium. Retinoic acid-treated cells occupied greater areas on the culture dish surface, and the cross-sectional area of these cells, measured on dispersed cells by light-scatter flow cytometry, was 35 to 40% greater than that of control cells. The inducibility of 9-1C cells for AP activity decreased as the culture density increased. Cells of the 9-1C clone produced tumors when injected into male and female Fischer X Copenhagen F1 rats. No histological differences were detected between tumors grown in male and female rats. Although the tumors were poorly differentiated, primitive acinar-like structures were observed. Cells staining uniformly positive for AP activity were distributed randomly throughout the tumors. In the acinar-like structures, AP activity was localized only on the apical surfaces of the cells lining the lumens. This was also the site of enzyme activity in acini of the lateral component of the dorsolateral prostate, the source of the original R-3327 tumor. In the lateral prostatic component, AP activity was also found in the basal region of the acini, and the secretory material filling the lumens was strongly positive for the enzyme. These two regions of the tumor acini were negative for AP activity. With the exception of activity in capillaries at the basal surface, the acini of the dorsal component of the dorsolateral prostate were devoid of AP activity.
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PMID:Effect of retinoic acid on the growth and morphology of a prostatic adenocarcinoma cell line cloned for the retinoid inducibility of alkaline phosphatase. 661 77

The influence of retinoic acid on matrix-induced endochondral bone differentiation was determined. Retinoic acid was administered during discrete stages of endochondral bone formation, specifically, mesenchymal cell proliferation, chondrogenesis, bone formation, and mineralization. In retinoic acid-treated rats examined on day 3 following matrix implantation, biochemical markers for mesenchymal cell proliferation were about 50% of the controls. Chondrogenesis on day 7, assessed by 35 SO4 incorporation into proteoglycans, was 27% of the control. In addition, dissociative extraction of proteoglycans with 4.0 M guanidine-HCl and chromatography on Sepharose CL-2B revealed the synthesis of a smaller molecular weight proteoglycan when compared to controls which exhibited the cartilage-specific type. Osteogenesis and bone mineralization were monitored by alkaline phosphatase activity and 45Ca incorporation. On day 11 alkaline phosphatase activity was decreased by 40% and 45Ca incorporation was 48% of the control. These results revealed the multiple foci of the actions of excess vitamin A.
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PMID:Influence of vitamin A on matrix-induced endochondral bone formation. 665 48

We have previously reported [(1980) J. Biol. Chem. 255, 5999-6002] that retinoic acid inhibited growth and increased cyclic-AMP-dependent protein kinase activity in mouse melanoma cells. A variant melanoma line having depressed levels of cyclic-AMP-dependent protein kinase was not growth-inhibited by retinoic acid. In this report we describe the effect of retinoic acid on cyclic AMP binding proteins in B16 mouse melanoma cells. Using the technique of photoaffinity labeling, we found three major proteins of Mr 49 000, 52 000, and 55 000 which were specifically labeled with 8-N3-[32P]AMP in both control and treated cells. Based upon their molecular weight, relative affinity for 8-N3-[32P]AMP and comigration with standards, we have designated the 49 000-Mr and 55 000-Mr species as RI and RII respectively. The position of the intermediate band (Mr 52 000) was not affected by pre-incubation with ATP or alkaline phosphatase, and two-dimensional gel analysis indicated that it had the same pI as RI. Retinoic acid increased the 8-N3-[32P]AMP labeling of RI within 24 h, reaching a maximal six fold increase by 48 h. These increases were limited to the 40 000 X g supernatant fraction and occurred prior to any growth inhibition. By using increasing concentrations of 8-N3-cAMP we were able to construct a saturation curve for RI binding. Calculation of apparent Kd values from these curves showed nearly identical affinities for RI binding of 8-N3-cAMP from control and retinoic-acid-treated cells. Therefore we conclude that retinoic acid is increasing the amount of RI rather than altering its properties. Corroboration of these results was obtained by DEAE-cellulose chromatography. Peak I (corresponding to type I protein kinase) from retinoid-treated cells was increased about six fold in binding activity.
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PMID:The effect of retinoic acid on cyclic-AMP-binding proteins in mouse melanoma cells. 669 18

The effects of retinoic acid (RA) on osteoblastic differentiation and activity were studied in fetal rat calvaria cells cultured for up to 24 days. Fetal bovine serum used for the experiments was treated with an anion-exchange resin to remove endogenous RA. The depletion of RA in the treated serum was confirmed by high-performance liquid chromatography and tritiated RA tracing. Under the culture conditions employed, the continuous presence of RA for 14 days at 10(-9) mol/l or higher decreased both alkaline phosphatase (ALP) activity on day 12 and the number of bone nodules on day 14 in a dose-dependent manner. Short-term (24 h) exposure to RA at 10(-8) mol/l, which is a physiological concentration, decreased and increased the levels of ALP and osteopontin mRNA on day 6, respectively. Retinoic acid at 10(-8) mol/l also increased the level of osteocalcin mRNA on day 12. However, these effects were not obvious at later stages (days 18 and 24). At a high concentration (10(-6) mol/l), RA increased the level of osteopontin mRNA on day 6 and decreased the levels of ALP and osteocalcin mRNA irrespective of culture period. These results suggest that, at physiological concentrations, RA suppresses the differentiation of osteoprogenitor cells and regulates osteoblastic functions.
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PMID:Physiological concentrations of retinoic acid suppress the osteoblastic differentiation of fetal rat calvaria cells in vitro. 758 51

This study examines the molecular mechanisms of interaction between tumor necrosis factor alpha (TNF alpha) and retinoic acid on the expression of the alkaline phosphatase gene by rat clonal preosteoblastic cells. In this cell line, alkaline phosphatase mRNA was not constitutively expressed but was progressively induced by treatment with 1 microM retinoic acid, detectable by 6 h. Combining retinoic acid with 0.6 nM TNF alpha resulted in alkaline phosphatase mRNA appearing by 2 h, as well as enhanced expression above that observed with retinoic acid alone at 6, 12, and 24 h. Nuclear run-on analysis showed constitutive transcription of the alkaline phosphatase gene in control and TNF alpha-treated cells. At 4 h, retinoic acid, alone or combined with TNF alpha, increased alkaline phosphatase gene transcriptional rate by 2-fold. However, at 24 h, while no retinoic acid effect was retained, retinoic acid plus TNF alpha resulted in a 5-fold increase in alkaline phosphatase transcriptional rate. Examination of the distribution of nuclear alkaline phosphatase mRNA demonstrated that pre-spliced precursor mRNA was localized to the nuclear matrix in control and all treatment groups. Retinoic acid caused a time-dependent accumulation of mature, spliced alkaline phosphatase mRNA located in the non-matrix and cytoplasmic fractions, implying a post-transcriptional action of retinoic acid in nuclear processing and nucleocytoplasmic transport. Adding TNF alpha with retinoic acid greatly enhanced this effect, which was observed after 4 h, prior to any detectable interaction between TNF alpha and retinoic acid on gene transcription. In sharp contrast, only a negligible amount of nuclear processing occurred in control and TNF alpha-treated cells. This study reveals distinct interactions between TNF alpha and retinoic acid at post-transcriptional as well as transcriptional levels to regulate expression of the alkaline phosphatase gene in preosteoblasts.
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PMID:Tumor necrosis factor alpha facilitates nuclear actions of retinoic acid to regulate expression of the alkaline phosphatase gene in preosteoblasts. 772 5

Treatment of the cultured human breast-cancer cells BC-M1 with dexamethasone induced a placental-type alkaline phosphatase (ALP). Both the ALP activity and the mRNA level in the cells were increased. The induction of ALP activity by dexamethasone was time- and dose-dependent. The accumulation of ALP mRNA was inhibited by both actinomycin D and cycloheximide, indicating that its induction is a complex event and may involve other regulatory proteins. Retinoic acid showed opposing effects with dexamethasone on the expression of alkaline phosphatase. Retinoic acid (RA) and phorbol 12-myristate 13-acetate also substantially reduced the dexamethasone-induced expression of ALP. Studies on thermostability and sensitivity to various amino acid inhibitors indicated that the BC-M1 ALP is most similar to the placental form. Northern hybridization analysis also revealed that ALP mRNA transcripts in BC-M1 and term placenta are similar in size and are distinct from that of the placental-like mRNA transcript in choriocarcinoma cells. Analysis of the degradation of BC-M1 ALP mRNA showed a similar half-life of 27 h in the untreated and in dexamethasone- or RA-treated cells. These findings demonstrated that the induction of ALP in BC-M1 cells by dexamethasone is mainly due to the increase in the transcription of the ALP gene.
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PMID:Regulation of the expression of alkaline phosphatase in a human breast-cancer cell line. 794 40

Retinoic acid (RA) induces secretory differentiation in the wound epidermis of a regenerating amphibian limb. We investigated the role of individual RA receptor (RAR) types in the newt wound epidermis by introducing chimaeric RA/thyroid hormone (T3) receptors (chi alpha 1 and chi delta 1) that can be activated by T3. A biolistic particle delivery system was employed to transfect cells in the wound epidermis of a regenerating limb and approximately 10% of the cells in targeted surface areas expressed marker genes. Both chi alpha 1 and chi delta 1 were comparable in their ability to stimulate transcription of a synthetic reporter construct through a RA response element after activation with T3 in situ. This activation was also comparable to that obtained by the endogenous complement of RARs in the RA-treated, transfected wound epidermis. The RA-inducible WE3 antigen, a marker for secretory differentiation, which distinguishes the wound epidermis from normal skin (Tassava, R. A., Johnson-Wint, B. and Gross, J. 1986, J. Exp. Zool. 239, 229-240), was used to assess the functional role of chi alpha 1 and chi delta 1. Chimaeric receptors were transfected with an alkaline phosphatase marker gene, activated with T3, and the expression of both the marker and WE3 was analyzed by double-label immunofluorescence. Newt limbs transfected with chi delta 1 showed many double-labelled cells dependent on the presence of T3, whereas contralateral limbs transfected with an alkaline phosphatase marker lacking chimaeric receptor sequences did not.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Isoform-specific induction of a retinoid-responsive antigen after biolistic transfection of chimaeric retinoic acid/thyroid hormone receptors into a regenerating limb. 814 12


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