Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.1.1.17 (ornithine decarboxylase)
 6,351 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cholera toxin activated beef thyroid cyclic AMP-dependent protein kinase in a dose (0.2 to 8 microgram/ml)-related fashion. Thus, when beef thyroid slices were incubated with toxin (8 microgram/ml) for 90 minutes and then assayed for protein kinase, the activity ratio (i.e. -cyclic AMP/+cyclic AMP) increased from 0.32 +/- 0.02 to 0.77 +/- 0.06. The toxin (5 microgram/ml)-induced increase was abolished by inclusion of ganglioside GM1 in the incubation medium (I50, 0.7 microgram/ml), whereas, gangliosides GD1a and GT1 were without effect. In contrast, TSH-activated protein kinase was unaffected by ganglioside addition. Cholera toxin increased rat thyroid ornithine decarboxylase (ODC) activity in-vitro in a dose (0.1 to 10 microgram/ml)-related fashion [basal, 100 cf cholera toxin (10 microgram/ml), 1500 pmol 14CO2/g tissue/30 min]. The toxin (1 microgram/ml)- (but not TSH-) induced increase in ODC was abolished by inclusion of ganglioside Ga and GT1 were without effect. Cholera toxin stimulation of ODC was inhibited by indomethacin or iodide as are the stimulatory effects of TSH or dibutyryl cyclic AMP. These results demonstrate that although there are differences in the TSH and cholera toxin responses with respect to receptor (ganglioside) interaction, they nevertheless elicit similar intracellular responses in thyroid.
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PMID:Effects of cholera toxin on thyroid cyclic AMP-dependent protein kinase and ornithine decarboxylase activities. 22 45

Bilateral transection of the lateral fimbria, which disrupts partially the septo-hippocampal projections and results in partial hippocampal denervation, produced a significant increase in the ornithine decarboxylase (ODC) activity in the hippocampus. An increase occurred already 0.5 h after the operation and the activity remained intensified for at least 22 h after injury. The enzyme response was enhanced by a single dose of GM1 monosialoganglioside (30 mg/kg) administered directly after the operation. This enhancement, detected 2 h after the injury, persisted for at least 22 h after the operation. Lack of influence of GM1 ganglioside on ODC activity in the hippocampus of unlesioned animals allows us to ascribe the observed effect to the processes induced by the lesion. This study confirms the involvement of ODC in GM1 ganglioside neurotrophic effects produced in an injured brain.
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PMID:Early changes in ornithine decarboxylase activity in a partially denervated hippocampus of rats untreated and treated with GM1 ganglioside. 213 Jun 67

Unilateral injection of colchicine into the dentate gyrus, kainic acid into the CA3 pyramidal cell field, or cerebrospinal fluid into either site produced significant increases in ornithine decarboxylase (ODC) activity in both the injected and noninjected hippocampi. The magnitude as well as the time course of these changes varied with the cytotoxin, the site of injection, and whether or not animals had been pretreated with ganglioside GM1. The ganglioside regimen reduced the ODC response in the injected hippocampus but increased it on the side contralateral to the colchicine injection. In contrast, GM1 enhanced the ODC response produced by kainic acid in the injected but not the uninjected hippocampus. In a subsequent study morphometric analysis of the hippocampus revealed that pretreatment with GM1 did not alter the extent of hippocampal injury induced by either cytotoxin. These data indicate that the changes in ODC activity observed following hippocampal damage represent a complex set of biochemical changes that might serve to protect primary or secondary sites of insult and/or to promote either adaptive or maladaptive neural reorganization. Ganglioside GM1 altered the ODC response without minimizing the histopathological changes induced by the cytotoxins. The role of polyamines in neural, behavioral, and synaptic plasticity is currently under study.
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PMID:Destruction of specific hippocampal cell fields increases ornithine decarboxylase activity: modulation of the biochemical but not the histological changes by ganglioside GM1. 274 27

The 4 major ganglioside species, GM1, GD1a, GD1b and GT1b (200 micrograms/ml), were tested individually for the ability to stimulate neuronal trophic responses. The growth parameters measured were: morphologic changes, quantitated by computer-assisted morphometry of neurite length and number per soma, and metabolic changes, indicated by alterations in ornithine decarboxylase activity (ODC). In addition, the interaction of each ganglioside with nerve growth factor (NGF) was investigated with an NGF-responsive pheochromocytoma PC12 cell line and NGF-insensitive neuroblastoma Neuro-2a cultures. PC12 cells responded to gangliosides only in the presence of NGF (20 micrograms/ml): GM1 produced the greatest morphologic response, but did not alter metabolic levels; GT1b increased both parameters. The presence (5 micrograms/ml) or absence of NGF did not have an effect on the ganglioside-mediated morphologic responses of Neuro-2a cells to each species: GD1b elicited the greatest increase in neurite length, while GD1a and GT1b stimulated both length and number. In contrast, while GT1b alone was able to elevate ODC activity independently of NGF, the simultaneous exposure of Neuro-2a cultures to NGF and GM1 or GD1a resulted in a stimulation of cellular metabolism. These results indicate that each ganglioside species has a specific target action in the stimulation of different trophic responses and that performance in one category is not a predictor of the result in another. In addition, it is possible to confer a sensitivity to NGF by simultaneous treatment with specific gangliosides. This indicates that membrane gangliosides may modulate the actions of neurotrophic factors.
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PMID:Neuritogenic and metabolic effects of individual gangliosides and their interaction with nerve growth factor in cultures of neuroblastoma and pheochromocytoma. 370 79

In male rats, partial hemitransections but not 6-hydroxydopamine (6-OHDA)-induced lesions of the mesostriatal dopamine (DA) pathway produce after 7 days a marked and a modest increase of striatal putrescine and spermidine levels, respectively, on the lesioned side. Following chronic ganglioside GM1 treatment of partially hemitransected rats, an increase of striatal polyamine levels was observed also on the intact side. It is suggested that retrograde cell body changes produced by hemitransection may induce striatal ornithine decarboxylase activity and in this way increase striatal putrescine levels, favoring regenerative mechanisms. The increase of striatal polyamine levels by GM1 treatment on the intact side of both 6-OHDA and mechanically lesioned rats compared with intact unoperated rats may also reflect an increased synthesis of striatal polyamines.
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PMID:Effects of neurotoxic and mechanical lesions of the mesostriatal dopamine pathway on striatal polyamine levels in the rat: modulation by chronic ganglioside GM1 treatment. 393 84

Isolated epidermal cells were incubated with a variety of compounds known to interfere with or alter the ultrastructure of cell surface receptors, and the ability of 12-O-tetradecanoyl-phorbol-13-acetate (TPA) to bind to these cells and induce epidermal ornithine decarboxylase (ODC) activity was investigated. The alpha- and beta-adrenergic antagonists, phentolamine and propranolol, and the cholinergic antagonist, atropine, which competed effectively for the binding receptors of [3H]dihydro-alpha-ergocryptine, [3H]dihydroalprenolol, and [14C]acetylcholine, did not inhibit the induction of ODC activity by TPA or the specific binding of [3H]TPA to the cells. Neuraminidase treatments caused a time- and dose-related release of sialic acid from the cells and enhanced the stimulatory effect of cholera toxin on basal and TPA-induced ODC activities as much as the monosialoganglioside GM1. Neuraminidase and the other membrane-altering agents, fucosidase, galactosidase, galactose oxidase, phospholipases A2 and C, and NaIO4, were used alone and/or in various combinations in our studies. All treatments tested inhibited the specific binding of several 125I-labeled hormones and epidermal growth factor to the cells. In contrast, none of these treatments was able, in the same cell system, to affect either the binding or the biological activity of TPA. Therefore, these results suggest that the primary interaction of TPA at the plasma membrane level as well as its biological effect in the intact cell do not proceed through adrenergic or cholinergic receptors and do not require the integrity of the cell surface glycoconjugates and phospholipids. In addition, the inhibitory effect of retinoic acid on TPA-induced ODC activity remained unaffected by some of the above treatments, suggesting that retinoic acid is unlikely to interfere with TPA interactions at the plasma membrane level.
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PMID:Effects of cell surface receptor-altering agents on the binding and biological activity of 12-O-tetradecanoylphorbol-13-acetate in isolated epidermal cells. 717 13

The effect of difluoromethylornithine (DFMO), an irreversible inhibitor of ornithine decarboxylase (ODC), the rate limiting enzyme of polyamine biosynthesis, and its combined action with GM1 ganglioside, was studied on the GFAP content in a model of remote astrogliosis evoked in the hippocampus by lateral fimbria transection. DFMO markedly suppressed hippocampal gliosis as measured by GFAP immunoblotting seven days postsurgery. Combined treatment with DFMO and GM1 ganglioside--a substance which alone also counteracts hippocampal gliosis, produced a stronger suppressive effect than DFMO. The results support the hypothesis of a causal link between lesion induced events: polyamine biosynthesis and astroglial reaction. Potentiation of the inhibitory effect of DFMO by GM1 ganglioside suggests that the latter does not act through the mechanism involving ODC suppression.
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PMID:Difluoromethylornithine counteracts lesion-induced astrogliosis in rat hippocampus: enhancement of inhibitory effect by combined treatment with GM1 ganglioside. 876 5