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

Dexamethasone, RO20-1724 and prostaglandin E1 all induced morphological alterations and increased the glial specific enzyme 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNP) in rat C6 glioma cells in culture. Morphological alterations consisted mainly in the development of astrocytelike changes. Increases in dexamethasone-induced CNP activity was time dependent. Dexamethasone reduced cell growth rate, depending on the concentration employed.
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PMID:Induction of 2',3'-cyclic nucleotide 3'-phosphohydrolase and morphological alterations in C6 glioma cells by dexamethasone, (3-butoxy-4-methoxybenzyl)-2-imidazolinone and prostaglandin E1. 624 33

Cultures of glial cell lines (C6) were exposed to 10-micromilligram Dexamethasone which is known to cause morphological differentiation and induction of 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNP) in these cells. Ethanol in a concentration of 1.5% abolished these responses, and at 1% diminished them.
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PMID:Alcohol inhibits morphological and biochemical differentiation of C6 glial cells in culture. 626 73

IGF-1 is an important factor for myelin synthesis and hence possesses therapeutic potential in treating demyelinating disease such as multiple sclerosis. However, IGF-1 poorly crosses the blood-brain barrier. In this study, we investigated the effects of the sex steroid progesterone and the glucocorticoid dexamethasone on regulation of the IGF-system in glial cells. By means of quantitative PCR analysis, we demonstrate that progesterone upregulates IGF-1, the type 1 IGF receptor and IGFBP-2 in primary rat astrocytes and both IGF-1 and IGFBP-6 in OLN-93 oligodendroglial progenitor cells. In contrast, dexamethasone showed a negative effect on expression of IGF-1, the type 1 IGF receptor and the respective IGF binding proteins in both cell types. In oligodendrocytes, the differentiation marker CNPase was positively regulated by progesterone and negatively regulated by dexamethasone. Further, oligodendroglial cell migration was enhanced approximately 4-fold by progesterone. This study implicates progesterone as a positive regulator of IGF-system in glial cells and demonstrates a further biological function of progesterone in oligodendrocyte biology, namely stimulation of progenitor cell migration. Dexamethasone, on the other hand, is a negative regulator of the IGF-system in glial cells.
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PMID:Progesterone and dexamethasone differentially regulate the IGF-system in glial cells. 1985 40