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)

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.
Acta Virol 1991 Sep
PMID:Relationship of 2',3'-cyclic nucleotide 3'-phosphohydrolase activity of large enveloped RNA viruses to host cell activity. 168 73

This study has dealt with the inhibition by lead of glutamine synthetase (GS) activity in homogenates of mixed glial primary cultures, 95% enriched in differentiating astrocytes. A 70% inhibition was observed with a lead concentration of only 2.5 microM. Prevention of the inhibition by addition of EDTA or dithiothreitol is compatible with the conclusion that the effect is mediated by binding of lead ion to sulfhydryl moieties of the enzyme. Among several other cations tested, only mercury, which has a similarly high binding affinity for sulfhydryl moieties, inhibited the enzyme. The inhibitory effect of lead was relatively specific, since no inhibition of another astrocytic marker enzyme, lactate dehydrogenase, of the oligodendroglial marker enzyme, 2',3'-cyclic nucleotide 3'-phosphohydrolase, or of the plasma membrane marker, Na,Ka-ATPase, was observed with concentrations of lead that produced a 70% decrease of GS. Because of the critical role of GS in regulation of extracellular glutamate, the findings raise the possibility that glutamate-induced neuronal injury is involved in the genesis of the cognitive defects associated with chronic low-level lead exposure in young children.
Brain Res Dev Brain Res 1990 Sep 01
PMID:Glutamine synthetase activity of developing astrocytes is inhibited in vitro by very low concentrations of lead. 197 58

Developing cultures of dissociated cerebral hemispheres obtained from 18-day-old embryonic rats synthesized, or activated, a myelin-related enzyme, 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNPase). This increase in activity coincided with the onset of myelination. The presence of CNPase in oligodendrocytes and myelin was demonstrated using immunocytochemical staining techniques. Myelinated axons and myelin sheaths were clearly made visible by electron microscopy of 28-day-old cultures.
Cell Struct Funct 1985 Sep
PMID:Myelin formation in dissociated cell cultures of rat embryonic cerebral hemispheres. 299 90

The direct influence of L-3,3',5-triiodothyronine (T3) on the development of 2',3'-cyclic nucleotide 3'-phosphohydrolase (EC 3.1.4.37, CNPase) is demonstrated by using an in vitro culture system of dissociated embryonic mouse brain cells. Serum from a thyroidectomized calf, which contained low levels of T3 (31 ng/100 ml), and thyroxine, T4 (less than 1 micrograms/ml), was used in the culture medium in place of normal calf serum (T3, 103 ng/100 ml; T4, 5.7 micrograms/ml) to render the culture responsive to exogenously added T3. The lower levels of enzyme activity observed in the presence of such a deficient medium could be restored to normal values by T3 supplementation. Half-maximal effect was obtained with 2.5 X 10(-9) M-T3. Three days of hormone treatment resulted in the maximal stimulation of CNPase. T4 was less effective in inducing CNPase activity and the inactive analog of the hormone, reverse T3 (3,3',5'-T3) was ineffective. The morphological appearance of the cells was characterized by deformed (smaller size and less in number) reaggregates in the cultures, lacking hormone.
J Neurochem 1981 Sep
PMID:Investigations on myelination in vitro: regulation of 2,3'-cyclic nucleotide 3'-phosphohydrolase by thyroid hormone in cultures of dissociated brain cells from embryonic mice. 626 53

Using data derived from peptide sequencing of p68/70, a protein doublet induced during optic nerve regeneration in goldfish, we have isolated cDNAs that encode RICH (regeneration-induced CNPase homolog) from a goldfish regenerating retina cDNA library. The predicted RICH protein comprises 411 amino acids, possesses a pI of 4.48, and shows significant homology to the mammalian myelin marker enzyme 2',3'-cyclic-nucleotide 3'-phosphodiesterase (CNPase; EC 3.1.4.37). The mRNA encoding RICH was demonstrated, by both Northern blot analysis and RNase protection assays, to be induced as much as 8-fold in regenerating goldfish retinas at 20 days after nerve crush. Analysis of total RNA samples from various tissues showed a broad distribution of RICH mRNA, with the highest levels observed in gravid ovary. The data obtained strongly suggest that RICH is identical or very similar to p68/70. The molecular cloning of RICH provides the means for a more detailed analysis of its function in nerve regeneration. Additionally, the homology of RICH and CNPase suggests that further investigation may provide additional insight into the role of these proteins in the nervous system.
Proc Natl Acad Sci U S A 1995 Sep 12
PMID:Isolation of cDNA clones encoding RICH: a protein induced during goldfish optic nerve regeneration with homology to mammalian 2',3'-cyclic-nucleotide 3'-phosphodiesterases. 756 86

We have previously established that 21-day-old postnatal rat oligodendrocytes, maintained in monolayer culture and subjected to 6 h of hypoxia, show reversible inhibition of synthesis of alpha-hydroxy fatty acid and myelin basic protein but a dramatic induction of a 22-kDa protein, suggesting that this is a good model to study the mechanism of CNS demyelination caused by hypoxic injury. We now report that hypoxia also dramatically inhibits the basal protein kinase C-mediated phosphorylation of myelin basic protein and myelin 2',3'-cyclic nucleotide phosphohydrolase by 80%, but that the inhibition of phosphorylation can be reversed by addition of a protein kinase C activator, phorbol 12-myristate 13-acetate. The mechanism of action appears to involve the uncoupling of signal transduction at a site before phospholipase C, because hypoxia did not affect protein kinase C activity or its translocation to the membrane fraction. The most potent activator of phospholipase C (as measured by inositol phosphate release) was carbachol (muscarinic M1 receptor agonist), followed by L-phenylephrine (alpha 1-adrenergic receptor agonist) in normal oligodendrocytes. Excitatory amino acids and histamine were ineffective. Hypoxia for 6 h completely inhibited both muscarinic and alpha 1-adrenergic receptor-mediated inositol monophosphate release but did not affect phospholipase D-coupled phosphatidylethanol production in response to carbachol. We therefore conclude from this and earlier work that early, reversible changes in oligodendrocyte metabolism result not simply from ATP depletion, but may specifically target GTP binding protein-mediated processes.
J Neurochem 1993 Sep
PMID:Effects of hypoxia on oligodendrocyte signal transduction. 768 39

Bovine splenic nerve was used as a source of axolemma-enriched fractions derived from mammalian unmyelinated axons. By electron microscopy, splenic nerve consisted entirely of fascicles of unmyelinated axons and associated Schwann cells. The epineurium and blood vessels were stripped from the dissected nerve, which was then homogenized followed by preparation of a microsomal fraction by differential centrifugation. The microsomes were fractionated on a 10% to 40% continuous sucrose gradient. The individual fractions were combined into six fractions based on sucrose concentration and each fraction was analyzed for membrane markers. The 20% to 23% region of the sucrose gradient was enriched approximately sevenfold in acetylcholinesterase activity and twofold enrichment in saxitoxin binding activity was noted in the same fraction. Relative to other microsomal fractions, this same fraction was less enriched in a microsomal marker (cytochrome c reductase) and only moderately enriched in the activity of a myelin membrane marker (2',3' cyclic nucleotide 3' phosphohydrolase, CNPase). Polyacrylamide electrophoresis of the axolemma-enriched fraction revealed five prominent peptides ranging in molecular weight from 40 kDa to 130 kDa. Lipids, comprising 59.4% of the dry weight, were enriched in cholesterol and sphingomyelin, consistent with the origin from a peripheral nervous system (PNS) plasma membrane. On a molar basis, the major gangliosides were G(T1b), G(D1a), and G(M1). As a whole, these molecular characteristics are consistent with the origin of the axolemma-enriched fraction in the unmyelinated splenic nerve axons. This membrane preparation should prove useful in future studies of the myelinogenic potential of mammalian unmyelinated axolemma.
J Neurosci Res 1999 Sep 01
PMID:Isolation and characterization of unmyelinated axolemma from bovine splenic nerve. 1046 91

To link the presence of intrathecal virus-specific oligoclonal immunoglobulin G (IgG) in multiple sclerosis patients to a demyelinating activity, aggregating rat brain cell cultures were treated with antibodies directed against two viruses, namely, rubella (RV) and hepatitis B (HB). Anti-RV antibodies in the presence of complement decreased myelin basic protein concentrations in a dose-dependent manner, whereas anti-HB antibodies had no effect. A similar but less pronounced effect was observed on the enzymatic activity of 2',3'-cyclic nucleotide 3'-phosphohydrolase, which is enriched in noncompact membranes of oligodendrocytes. These effects were comparable to those in cultures treated with antibodies directed against myelin oligodendrocyte glycoprotein (MOG), previously found to be myelinotoxic both in vitro and in vivo. Sequence homologies were found between structural glycoprotein E(2) of RV and MOG, suggesting that demyelination was due to molecular mimicry. To support the hypothesis that demyelination was caused by anti-RV IgG that recognized an MOG epitope, we found that anti-RV antibodies depleted MOG in a dose-dependent manner. Further evidence came from the demonstration that anti-RV and anti-MOG IgG colocalized on oligodendrocyte processes and that both revealed by Western blot a 28 kDa protein in CNS myelin, a molecular weight corresponding to MOG. These findings suggest that a virus such as RV exhibiting molecular mimicry with MOG can trigger an autoimmune demyelination.
J Neurosci Res 2001 Sep 01
PMID:Antibodies directed against rubella virus induce demyelination in aggregating rat brain cell cultures. 1153 29

Lineage uncommitted pluripotent stem cells reside in the connective tissue of skeletal muscle. The present study was carried out with pluripotent stem cells (PPSCs) isolated from 6-month old rat muscle. Before differentiation, these cells were vimentin+, CD90+, CD45-, and varied in their expression of CD34. The PPSCs were expanded as non-adherent aggregates under similar conditions to those used to generate neurospheres from embryonic or neural stem cells. The PPSC-derived neurospheres were positive for nestin, an early marker present in neuronal precursors, and expressed the two alternative mRNA forms of the neuroectodermal marker Pax-6, as well as mRNA for Oct-4, a gene related to the pluripotentiality of stem cells. To confirm their neural potential, PPSC-derived neurospheres were plated on coated coverslips under varying conditions: Neurobasal medium with N2 or B27, and either NT3 or BDNF. After 4-6 days the cells expressed neuronal (Tuj1+, NF68), astrocytic (GFAP) and oligodendrocytic (MOSP+, MBP+) markers, both by immunocytochemistry and RT-PCR. In addition, PPSCs were cultured as monolayers under adherent conditions, exposed to growth factors and defined differentiating conditions for 5 hr, and subsequently kept for 2 days in a maturation medium. At this point they gave rise to a mixed population of early neural progenitors (Nestin+ or NG2+), immature and mature neurons (Tuj1+ and NF145+) and myelin producing oligodendrocytes (CNPase + and MOSP+). Our study shows that PPSCs present in adult muscle can overcome germ lineage restrictions and express the molecular characteristics of brain cells. Therefore, PPSCs isolated from adult muscle could provide a novel source for autologous cell replacement in neurodegenerative and demyelinating diseases.
J Neurosci Res 2002 Sep 15
PMID:Neuronal differentiation of stem cells isolated from adult muscle. 1220 82

Loss of arginase I (AI) results in a metabolic disorder characterized by growth retardation, increased mental impairment and spasticity, and potentially fatal hyperammonemia. This syndrome plus a growing body of evidence supports a role for arginase and arginine metabolites in normal neuronal development and function. Here we report our initial observations of the effects of AI loss on proliferation and differentiation of neural stem cells (NSCs) isolated from the germinal zones of embryonic and newborn AI knockout (KO) mice compared with heterozygous (HET) and wild-type (WT) control animals. By using both short and long-term proliferation assays (3 and 10 days, respectively), we found a 1.5-2-fold increase in the number of KO cells compared with WT. FACS analysis showed an increase in KO cells in the synthesis phase of the cell cycle vs. WT cells. After NSC differentiation, AI-deficient cells expressed beta-tubulin, SMI81 (SNAP25), glial fibrillary acidic protein, and CNPase, which are markers consistent with neurons, astrocytes, and oligodendrocytes. Many KO cells exhibited a more mature morphology and expressed mature neuronal markers that were decreased or not present in HET or WT cells. Limited, comparative expression array and quantitative RT-PCR analysis identified differences in the levels of several mRNAs encoding structural, signaling, and arginine metabolism proteins between KO and WT cells. The consequence of these changes may contribute to the differential phenotypes of KO vs. WT cells. It appears that AI may play an important and unanticipated role in growth and development of NSCs.
J Neurosci Res 2006 Sep
PMID:Loss of arginase I results in increased proliferation of neural stem cells. 1677 51


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