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:4.1.1.17 (ornithine decarboxylase)
6,351 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In Neurospora cells grown on minimal medium, most of the large ornithine pool is found in osmotically sensitive organelles, the "vesicles." In this paper kinetic studies on the compartmental behavior of ornithine and its derivatives are reported. Analysis of the metabolism of a 10(-7) M pulse of uniformly labeled L-[14C] ornithine supports the following conclusions: (a) Over 98% of the cellular ornithine is in the vesicles. (b) The amount of ornithine normally in the cytosol is about 0.3% of the cellular ornithine, as shown by the kinetics of incorporation of 14C into putrescine via the cytosolic enzyme, ornithine decarboxylase (EC 4.1.1.17). (c) Mitochondria, the site of ornithine synthesis, contain about 1% of the cellular ornithine, as demonstrated by the kinetics of incorporation of 14C into citrulline via the mitochondrial enzyme, ornithine transcarbamylase (EC 2.1.3.3). (d) Considerable ornithine exchange, and a net efflux of ornithine, takes place across the mitochondrial membrane. (e) Ornithine aminotransferase (EC 2.6.1.13), a catabolic enzyme, may have a special relation to the cell membrane in cells grown in minimal medium. This enzyme uses ornithine efficiently while it enters from the medium, but very poorly after all the [14C] ornithine is within the cell. (f) Citrulline and proline are not compartmented with respect to the enzymes using them. (g) In contrast, arginine is distributed such that over 99% is in vesicles. We suggest that the vesicles; with their ability to sequester ornithine and arginine, are potentially significant in regulation.
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PMID:Compartmental behavior of ornithine in Neurospora crassa. 13 43

Two auxotrophs of Neurospora crassa have been isolated that give a positive growth response to putrescine, spermidine or spermine. One of the mutants is deficient in ornithine decarboxylase activity and has been designated put-I. Both mutants map on linkage group VR, fail to complement and are infertile when crossed to one another, indicating that they are probably alleles. A putrescine auxotroph is incapable of suppressing a pro-4 mutant. The isolation of the mutants confirms that putrescine is an essential factor the normal growth of the organism, and is synthesized via a single pathway in Neurospora.
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PMID:Isolation of putrescine-requiring mutants of Neurospora crassa. 14 23

Administration of the beta-agonist isoproterenol to rats caused a sharp increase in the influx rate of taurine into the heart, but had no effect on the rate of biosynthesis of taurine in the heart. Influx rates of other amino acids were also stimulated, the distribution ratios, (dpm/g heart)/(dpm/ml plasma), of beta-amino acids being 3--4 times higher than alpha-amino acids. The doses of isoproterenol employed induced cardiac hypertrophy, but the stimulation of taurine influx appeared to be an independent phenomenon, in that near maximum stimulation of influx was achieved prior to stimulation of ornithine decarboxylase activity. Reserpine treatment also produced stimulation of taurine influx with no effect on biosynthesis. These results indicate a close connection between increased sympathomimetic activity and increased influx of amino acids.
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PMID:The effects of isoproterenol on taurine concentration in the rat heart. 14 63

The standard mixed lymphocyte culture assay, which measures the incorporation of [3H]thymidine into DNA, usually requires 5 days. We describe a more rapid assay based on changes in the activity of ornithine decarboxylase. An increase in the activity of ornithine decarboxylase was observed in mixed lymphocyte cultures from genetically defined, major histocompatibility complex (MHC)-nonidentical miniature swine as early as 18 hr after plating. No increase was found in mixed cultures from inbred MHC-identical animals. Similar results were obtained with the enzyme S-adenosylmethionine decarboxylase with the increase in activity starting at about 32 hr. There was a good correlation between the ornithine decarboxylase values at 18 hr and the results of the [3H]thymidine incorporation assay on day 5. Preliminary experiments with human lymphocytes revealed similar results.
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PMID:An enzymatic method permitting early determination of histocompatibility in mixed lymphocyte culture. 15 34

Strains of Escherichia coli K12 have been constructed which do not contain any of the polyamines normally present in a wild type strain, namely, 1,4-diaminobutane (putrescine) and spermidine. This phenotype arises as a consequence of the assembly into these strains of deletion mutations in speA (arginine decarboxylase), speB (agmatine ureohydrolase), speC (ornithine decarboxylase), and speD (adenosylmethionine decarboxylase). The polyamine-deficient strains grow indefinitely in the absence of polyamines but with a growth rate one-third of that found in the presence of polyamines. These strains can act as hosts for bacteriophages T4, T7, and f2, although the latter phage is poorly adsorbed; they can also maintain F' factors, ColE1 and P1 plasmids, and lysogeny by bacteriophage lambda. In contrast, the production of bacteriophage lambda in the absence of polyamines is strikingly decreased (greater than 99%) either after infection of a nonlysogen or after induction of a lysogen. A polyamine-deficient Hfr strain can transfer its chromosome to a recipient at a normal rate, but the number of recombinants observed in a cross is decreased approximately 300-fold. No such effect is observed when only the F- recipient strain in a cross is polyamine deficient.
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PMID:Mutants of Escherichia coli that do not contain 1,4-diaminobutane (putrescine) or spermidine. 15 6

Both exposure to cold and administration of aminophylline result in rapid increases in cyclic adenosine monophosphate (cyclic AMP) in the adrenal medulla and adrenal cortex. These increases are followed by dramatic increases in ornithine decarboxylase activity is due to new enzyme systhesis. The data suggest that the decarboxylase activity is regulated by an increase in cyclic AMP.
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PMID:Ornithine decarboxylase activity: control by cyclic nucleotides. 16 86

We studied the effects of TSH on rat thyroid ornithine decarboxylase (ODC) activity. After 1 day of goitrogen treatment, there was an abrupt fall in serum triiodothyronine (T3) a rise in circulating TSH, and a dramatic increase in thyroid ODC activity. Despite the continued rise in TSH and progressive increase in thyroid gland size with further treatment, thyroid ODC activity declined on the third day and remained at submaximal levels. Thyroid ODC activity was also stimulated in a dose-related manner by administration of exogenous TSH. Little TSH effect was noted before 3 h. Maximal ODC activity occurred between 4 and 5 h. The TSH stimulation of ODC could be inhibited by pretreatment with actinomycin D or cycloheximide, suggesting that the increase in ODC activity requires new RNA and protein synthesis. Although pretreatment with agents that alter microtubule structure (e.g., colchicine and vinblastine) prevent stimulation of ODC activity by TSH, additional data suggest, but do not confirm, that hrmone secretion and ODC activation may be dissociable. Further studies were undertaken to determine whether cyclic AMP (cAMP) or prostaglandins played any role in the regulation of thyroidal ODC activity. Dibutyryl cAMP, alone, or together with aminophylline, did not stimulate thyroidal ODC activity in dosages which concomitantly stimulated adrenal enzyme activity. Likewise, prostaglandin E2 (PGE2) did not stimulate thyroidal ODC activity, but did stimulate adrenal enzyme activity in a dose-related manner. However, pre-treatment of rats with inhibitors of prostaglandin synthesis prevented the activation of thyroidal ODC BY TSH. One inhibitor, indomethacin, attenuated the TSH stimulation of enzyme activity in a dose-related manner. Indomethacin pretreatment also resulted in approximately a 10-fold decrease in thyroidal prostaglandin levels. Exogenous PGE9, in dosages as high as 500 pg, did not overcome the inhibitory effect of indomethacin on ODC activation. Although the precise role for endogenous prostaglandins remains to be defined, it does appear that a reduction in thyroidal prostaglandins prevents activation of the enzyme by TSH.
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PMID:Regulation of thyroid ornithine ornithine decarboxylase (ODC) by thyrotropin. I. The rat. 16 59

A mixture containing glucagon and thyroid hormone was previously devised that enhances markedly nuclear DNA replication and mitosis in the parenchymal liver cells of the unoperated rat. It is now shown that the glucagon of the stimulatory solution can be completely replaced by a mixture of a butyryl derivative of cyclic adenosine 3':5'-monophosphate and theophylline. Cyclic guanosine 3':5'-monophosphate and its butyryl derivatives and insulin and high levels of glucose are inactive. The inactivity of N2-monobutyryl cyclic guanosine 3':5'-monophosphate cannot be ascribed to rapid breakdown in the animal or to the impenetrability of the liver cell since the coumpound elevates the rate of hepatic amino acid transport and the activity of ornithine decarboxylase. The observation of others (MacManus, J.P., Franks, D.J., Youdale, T. & Braceland, B.M. (1972) Biochem. Biophys. Res. Commun. 49, 1201-1207) that the level of cylcic adenosine 3':5'-monophosphate is raised during most of the prereplicative period after 70% hepatectomy is confirmed. The evidence supports a positive role for adenosine 3':5-monophosphate in regulating DNA synthesis in the liver.
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PMID:Cyclic adenosine 3':5'-monophosphate and the induction of deoxyribonucleic acid synthesis in liver. 16 78

Chinese hamster V79 cells were synchronized by mitotic selection, which resulted in approximately 95% synchrony. The adenosine 3':5'-cyclic monophosphate level was elevated within 3 hr (G1 phase) and reached a level 2-fold higher than in early G1 within 6 hr (early S phase). An increase in ornithine decarboxylase activity (6-ornithine carboxy-lyase, EC 4.1.1.17), the initial enzyme in the polyamine biosynthetic pathway, was detected within 4 hr and was maximal at 8 hr. Since about 20% of the cells were labeled with [3-H]thymidine at 4 hr, ornithine decarboxylase exhibits cell-cycle specific activity starting in late G1 and continuing through middle S phase. The activity of S-adenosylmethionine decarboxylase (S-adenosyl-L-methionine carboxylase, EC 4.1.1.50) increased within 5 hr, i.e., early S phase. It is suggested on the basis of these data and other studies discussed herein that the increase in ornithine decarboxylase activity, which parallels closely the elevation in cyclic AMP, is an example of adenosine 3':5'-cyclic monophosphate-mediated protein synthesis.
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PMID:Cell cycle specific fluctuations in adenosine 3':5'-cyclic monophosphate and polyamines of Chinese hamster cells. 16 12

The mechanism of action of adrenocorticotrophin (ACTH) stimulation of rat adrenal orticotrophin (ACTH) stimulation of rat adrenal ornithine decarboxylase activity was investigated. ACTH induction or ornithine decarboxylase activity was not prevented by administration of drugs that inhibit adrenal steroid biosynthesis. A dose of ACTH that produced maximal levels of adrenal cyclic AMP did not induce ornthine decarboxylase activity. Ovine growth hormone, which caused no increase in adrenal cyclic AMP, stimulated adrenal ornithine decarboxyase activity. These observations suggest that the increase in adrenal ornithine decarboxylase activity stimulated by ACTH is not dependent upon steroidogenesis, nor is it dependent on the early peak of cyclic AMP, although it may be influenced by the sustained levels of tissue cyclic AMP that follow the administration of large doses of ACTH. Furthermore, it appears there may be a pathway of ornithine decarboxylase activation in the adrenal which is entirely independent of cyclic AMP mediation. The effects of hypophysectomy on adrenal ornithine decarboxylase response to ACTH were examined. In rats given ACTH 16 h after hypophysectomy, the increase in ornithine decarboxylase activity was delayed when compared with the response in animals given ACTH 1 h after hypophysectomy. Actinomycin D given during the first 3 h after ACTH in the 16 h hypophysectomized rat abolished the expected increase in ornithine decarboxylase activity. Thereafter, a progressive increase in ornithine decarboxylase activity was observed as the interval between ACTH and Actinomycin D administration was further increased. In contrast, Actinomycin D administered 15 min before ACTH in the 1 h hypophysectomized rat had no effect on the subsequent increase in ornithine decarboxylase activity, and actually progressively enhanced the response the longer its administration after ACTH was delayed. Cycloheximide abolished the response to ACTH in both the 1 h and the 16 h hypophysectomized rat. Thus, it appears that ACTH stimulates a post-transcriptional mechanism regulating ornithine decarboxylase activity in the acutely hypophysectomized animal, whereas, in the chronically hypophysectomized rat, ACTH must first stimulate transcription of new messenger RNA which is involved in regulation of adrenal ornithine decarboxylase synthesis.
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PMID:The mechanism of ACTH stimulation of adrenal ornithine decarboxylase activity. 16 25


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