Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.4.37 (CNPase)
539 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have established permanent cell lines from the optic nerve of the rat with a temperature sensitive immortalizing oncogene (Simian Virus 40 large T-antigen carrying both the tsA58 and U19 mutations). The oncogene was transduced into primary cultures via a replication deficient retrovirus, and infected cells were selected with the antibiotic G418. A clonal cell line (tsU19-5) displayed some properties of oligodendrocyte precursors: it proliferated, bound the monoclonal antibody A2B5 (which recognizes minor ganglioside species), and expressed the intermediate filament vimentin and the enzyme 2',3'-cyclic-nucleotide 3'-phosphodiesterase (CNP) at 33 degrees C (the permissive temperature for the oncogene). At 39 degrees C (the non-permissive temperature), some cells had the potential to differentiate further, and expressed several oligodendrocyte specific components: galactocerebroside, myelin basic protein, proteolipid protein and CNP. These results suggest that conditional oncogenes can establish neural precursor cell lines which are still capable of differentiation in vitro.
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PMID:An oligodendrocyte precursor cell line from rat optic nerve. 162 12

Psychosine cytotoxicity was tested as to its effects on rat C6 glioma cells. At a low concentration--below 40 microM--psychosine appeared to stimulate cell proliferation. Above the concentration range of 40 microM-60 microM, however, it showed a cytotoxic effect. When phorbol ester (PDB) or dimethylsulfoxide (DMSO) was supplemented to cultures being exposed to psychosine, the total number of live cells, protein content and CNPase activity dramatically increased as compared with the levels in cultures treated with psychosine alone. The results of these basic studies suggest another approach as to therapy for globoid cell leukodystrophy.
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PMID:Psychosine cytotoxicity toward rat C6 glioma cells and the protective effects of phorbol ester and dimethylsulfoxide: implications for therapy in Krabbe disease. 165 28

Rat embryos in utero at 10 days of gestation (gd) were exposed to the intensity of 2.5 W/cm2 (SATA) of 1 MHz continuous-wave ultrasound for 5 min. The right uterine horn was exteriorized, exposed to the ultrasound beam, and then reinserted into the abdominal cavity. Embryos from the unexposed left uterine horn served as controls. The cerebral hemispheres of each fetus were removed and analyzed for enzymatic activity at four different stages of development. There was an increase in the temperature at the surface of the intact uterus during the ultrasound exposure. No gross anatomical malformations were observed in the exposed embryos. There were no differences in brain weight or protein content between exposed and control fetuses. However, the ultrasound exposure caused a transient decrease in acetylcholine esterase and 2',3'-cyclic nucleotide phosphohydrolase activities of the insonated fetal brains compared to the control brains. Because of the relatively high temporal-average intensity, the relatively large volume of tissue exposed, and the minimal sound path through tissue, the biochemical changes observed in this experiment would be unlikely to occur in clinical examinations.
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PMID:Reversible biochemical changes in the developing rat central nervous system following ultrasound exposure. 165 13

Insulin-like growth factor I (IGF-I) and high concentrations of insulin have been shown to stimulate an increase in the number of oligodendrocytes that appear in developing monolayer cultures of rat brain cells (McMorris et al., Proc Natl Acad Sci USA 83: 822-826, 1986; McMorris et al., Ann NY Acad Sci 605:101-109, 1990; McMorris and Dubois-Dalcq, J Neurosci Res 21:199-209, 1988). In the present study, we investigated whether IGF-I or insulin treatment induces a corresponding increase in the synthesis and accumulation of myelin. Aggregate cultures, established from 16-day-old fetal rat brains, were treated with either 100 ng/ml IGF-I or 5,000 ng/ml insulin and analyzed for the number of oligodendrocytes, activity of 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNP), total amount of myelin, and synthesis rate of myelin proteins. Cultures treated with IGF-I beginning on day 2 after explantation contained 35-80% more oligodendrocytes and had 60-160% higher CNP activity than controls when tested on day 13, 20, or 27. By day 27, treated cultures had 35-90% more myelin than controls. Similar results were observed in response to 5,000 ng/ml insulin, a concentration at which insulin binds to IGF receptors and acts as an analogue of IGF-I. The synthesis rate of myelin proteins was measured in experiments using 5,000 ng/ml insulin. When treatment was begun at day 20 rather than day 2, cultures did not exhibit an increased number of oligodendrocytes over control during the following 4-6 days.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin-like growth factor I stimulates oligodendrocyte development and myelination in rat brain aggregate cultures. 166 69

The myelin basic protein (MBPi) accounts for the main encephalitogenic antigen of the demyelinating encephalopathy, but other myelin elements also be noted by some articles. We tried to determine the relationship between W1 protein and the demyelinating encephalopathies. The 2',3'-cyclic nucleotide 3'-phospho-diesterase(CNPase, a gift from Dr. Yasuzo Tuskada) monoclonal antibody was used as a probe to study the W1 protein level in 5 different demyelinating encephalopathies and 2 normal adult brains with immunocytochemical technique. Two different demyelinating types of W1 protein level were found out. Type 1 showed the W1 protein level parallel with demyelinated feature in general pathology whereas the type 2 showed demyelinated in the general pathology but the W1 protein level was normal in the immunocytochemical study. Multiple system degeneration, Binswanger's disease and postvaccinal encephalopathy of type B encephalitis belong to type 1 and multiple sclerosis and Balo's concentric sclerosis belong to type 2. These results might indicate the different pathogenesis of demyelinating encephalopathies.
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PMID:[Demyelinating elements of demyelinated encephalopathy]. 168 19

Purified virions of the large RNA viruses show 2',3'-cyclic nucleotide 3'-phosphohydrolase (3'-CNPase) activity. The 3'-CNPase activity is virion-associated and stimulated by their treatment with nonionic detergents. Cytopathic viruses such as influenza A2 (Singapore/57), NDV, and VSV showed the specific activity of a virion-associated 3'-CNPase equal to or lower than the specific activity of host cell enzyme. Retroviruses are an example of extreme relationship of 3'-CNPase to virion. With the AMV-BAI-A associated enzyme activity increased after Triton X-100 treatment ten times more than that associated with other viruses examined. The specific activity of virus-associated 3'-CNPase was 16-28 times higher than that in chick myeloblasts. BLV showed a very low enzyme activity. The correlation between the activity of cellular 3'-CNPase and virus yield showed that 3'-CNPase could belong to cellular factors influencing virus replication.
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PMID:Relationship of 2',3'-cyclic nucleotide 3'-phosphohydrolase activity of large enveloped RNA viruses to host cell activity. 168 73

Schwann cells, on receiving the correct signal, will encircle an axon and wrap it with a myelin sheath. To begin examining some of the mechanisms underlying the process of myelination in vitro, we isolated Schwann cells from the sciatic nerves of neonatal rats and generated large cell populations with cholera toxin. The immunological and biochemical properties of these secondary Schwann cells were characterized after five to seven passages in the absence of axonal contact. These cells continued to express antigens found in both myelinating (P0 and 2',3'-cyclic nucleotide phosphohydrolase) and nonmyelinating cells in vivo (A5E3 and glial fibrillary acidic protein) in addition to the markers common to both types of cells (Ran-1, 217c, S-100, and laminin). Biochemical analyses showed that these cells synthesize the very-long-chain fatty acids (22-26 carbon atoms) found in myelin membranes. Moreover, the enzymes required for the synthesis of myelin glycolipids (including sphingosine acyltransferase, UDP-galactose:ceramide galactosyltransferase, and cerebroside sulfotransferase) were still active, and metabolic labeling studies showed that galactocerebroside and sulfatide were synthesized even though the galactocerebroside pool was insufficient to be detected by immunostaining. Secondary Schwann cells also synthesized four species of myelin basic protein and the major structural glycoprotein in myelin, P0. The pathway necessary for glycosylation of P0 protein remained active, and an analysis of the oligosaccharide chain revealed that approximately 70% was processed to a complex form. In summary, we found that secondary Schwann cells still express most of the immunological markers of differentiated cells and continue to synthesize low levels of myelin components. Therefore, Schwann cells do not dedifferentiate in culture, as previously believed.
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PMID:Evidence that secondary rat Schwann cells in culture maintain their differentiated phenotype. 169 82

A monoclonal antibody (8-18C5) directed against myelin/oligodendrocyte glycoprotein (MOG) induced demyelination in aggregating brain cell cultures. With increasing doses of anti-MOG antibody in the presence of complement, myelin basic protein (MBP) concentration decreased in a dose-related manner. A similar, albeit less pronounced, effect was observed on specific activity of 2',3'-cyclic nucleotide 3'-phosphohydrolase. In the absence of complement, anti-MOG antibody did not induce detectable demyelination. In contrast to the effect of anti-MOG antibody and as expected, anti-MBP antibody did not demyelinate aggregating brain cell cultures in the presence of complement. These results provide additional support to the suggestion that MOG, a quantitatively minor myelin component located on the external side of the myelin membrane, is a good target antigen for antibody-induced demyelination. Indeed, they show that a purified anti-MOG antibody directed against a single epitope on the glycoprotein can produce demyelination, not only in vivo as previously shown, but also in cultures. Such an observation has not been made with polyclonal antisera raised against purified myelin proteins like MBP and proteolipid protein, the major protein components of the myelin membrane, or myelin-associated glycoprotein. These observations may have important implications regarding the possible role of anti-MOG antibodies in demyelinating diseases.
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PMID:Demyelination induced in aggregating brain cell cultures by a monoclonal antibody against myelin/oligodendrocyte glycoprotein. 169 40

Cells resembling oligodendrocytes are sometimes seen within reactive astrocytes in fresh lesions in multiple sclerosis. Using immunostained paraffin and epoxy sections of fresh plaques obtained at autopsy from a series of cases of short clinical duration, it was found that small cells with round nuclei are commonly observed within reactive astrocytes in some hypercellular plaques and that these cells are phenotypically undifferentiated oligodendrocytes, i.e., nonmyelinating cells expressing intensely the oligodendrocyte determinants 2',3'-cyclic nucleotide 3'-phosphohydrolase and the carbohydrate epitope present on the family of cell adhesion molecules recognized by monoclonal antibody HNK-1. They also stain positively for IgG. This unusual astrocyte-oligodendrocyte interaction, which appears to be restricted to nonmyelinating oligodendrocytes in lesions of several weeks' to several months' duration, has not been described during normal oligodendrocyte differentiation or in experimental central remyelinating lesions. It bears some resemblance, however, to a pattern of slow oligodendrocyte destruction seen previously in organotypic perinatal central nervous tissue cultures exposed to multiple sclerosis serum. It is concluded that the evolution of some multiple sclerosis lesions early in the course of the disease is associated with abnormal binding and/or destruction of newly generated oligodendrocytes by reactive astrocytes. These observations raise new questions concerning mechanisms underlying failed remyelination in multiple sclerosis, including the novel possibility of an immune response directed against a developmentally restricted oligodendrocyte antigen.
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PMID:Interaction of astrocytes and newly formed oligodendrocytes in resolving multiple sclerosis lesions. 170 Jan 95

After lindane administration at several doses, brain myelin fractions of litters of male and female Wistar rats show a significant diminution of CNP (2',3'-cyclic nucleotide 3'-phosphodiesterase) activity. Furthermore, the immunohistochemical study of brains by means of a MBP (myelin basic protein) specific antibody reveals myelin deficits in some brain regions after lindane treatment. This loss of myelin protein is dose dependent. The deficit in myelin cannot be attributed to undernourishment of lindane-administered rats. This work shows the vulnerability of the developing central nervous system (CNS) to lindane and the correlation between a decrease in the CNPase activity and a deficit of MBP during the period of study of these animals.
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PMID:Effect of lindane on the myelination process in the rat. 170 14


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