Disease relevance of Cnp1

• Biochemical properties of cyclic nucleotide phosphodiesterase in metastasizing and nonmetastasizing rat mammary carcinomas [1].
• Analysis of cyclic nucleotide phosphodiesterase (PDE) activity in cellular fractions from cultured rat pheochromocytoma (PC12) cells has shown that the predominant hydrolytic activity in both cytosolic and particulate compartments is characteristic of a PDE II, the cGMP-activatable family of PDE isozymes [2].
• After removal of mitogens and addition of thyroid hormone, Rb stopped being expressed and CNPase expression was activated with a temporal course similar to that of oligodendrocytes infected with a control adenovirus [3].
• The relationship between cell density and the activity of 2':3'-cyclic nucleotide 3'-phosphohydrolase (CNP), an enzyme believed to be specific to oligodendroglial cells and myelin in the brain, has been studied in cultured C-6 glioma cells [4].
• CONCLUSIONS: In conclusion, this study shows that the natriuretic response to pharmacological doses of CNP and BNP is blunted in rats with cirrhosis [5].

Psychiatry related information on Cnp1

• The increase in locomotor activity was correlated with the suppression of CNPase activity [6].
• Differential changes in the expression of cyclic nucleotide phosphodiesterase isoforms in rat brains by chronic treatment with electroconvulsive shock [7].

High impact information on Cnp1

• Diurnal rhythm in rat pineal cyclic nucleotide phosphodiesterase activity [8].
• Here, we show a novel leptin signaling mechanism that requires phosphoinositide 3-kinase (PI 3-kinase)-dependent activation of cyclic nucleotide phosphodiesterase 3B (PDE3B) and subsequent suppression of cAMP levels [9].
• Calmodulin-stimulated cyclic nucleotide phosphodiesterase (PDE1C) is induced in human arterial smooth muscle cells of the synthetic, proliferative phenotype [10].
• cGMP-stimulated cyclic nucleotide phosphodiesterase regulates the basal calcium current in human atrial myocytes [11].
• Inhibitors of cyclic nucleotide phosphodiesterase isozymes type-III and type-IV suppress mitogenesis of rat mesangial cells [12].

Chemical compound and disease context of Cnp1

• Antihypertrophic effects of BNP and CNP are mediated through cyclic GMP-dependent protein kinase, but ANP can activate additional pathways independent of cyclic GMP to prevent adult cardiomyocte hypertrophy [13].
• Cyclic AMP (cAMP) is known to induce the activity of the myelin enzyme 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNP; EC 3.1.4.37) in C6 rat glioma cells [14].
• Theophylline, a cyclic nucleotide phosphodiesterase inhibitor, increases the rate of tyrosine aminotransferase (TAT) degradation in rat hepatoma tissue culture (HTC) cells [15].
• RESULTS: Ang II-stimulated increases in markers of hypertrophy, [3H]phenylalanine incorporation (to 136+/-3% of control, n=9) and c-fos mRNA expression (4.3+/-1.4-fold, n=5), were completely prevented by each of ANP, BNP or CNP [13].
• Suppression of arterial intimal hyperplasia by cilostamide, a cyclic nucleotide phosphodiesterase 3 inhibitor, in a rat balloon double-injury model [16].

Biological context of Cnp1

• Assignment of the 1H, 13C and 15N resonances of the catalytic domain of the rat 2',3'-cyclic nucleotide 3'-phosphodiesterase [17].
• Juxtanodin transfection promoted arborization of cultured OLN-93 cells and augmented endogenous CNPase expression and transport to the process arbors of cultured primary oligodendrocyte precursors [18].
• Subcellular localization of cyclic nucleotide phosphodiesterase type 10A variants, and alteration of the localization by cAMP-dependent protein kinase-dependent phosphorylation [19].
• A good correlation was found to exist between the dose that produced 50% of maximal induction and a combination of the activation constant for cyclic adenosine 3':5'-monophosphate-dependent protein kinase by the analog and its susceptibility to hydrolysis by cyclic nucleotide phosphodiesterase [20].
• The peptide bound to fluorescently labeled 5-dimethylaminonaphthalene-1-sulfonyl-calmodulin with a dissociation constant of 2.8 nM, and inhibited the calmodulin-dependent activation of cyclic nucleotide phosphodiesterase with an IC50 of 4.8 nM [21].

Anatomical context of Cnp1

• There was no age-related loss of CNPase immunoreactivity in glial cell bodies, possibly indicating de novo ensheathment of neurites [22].
• The Michaelis-Menten kinetic for CNPase in myelin obtained from control and Pb-treated rats was different [23].
• Interestingly, in addition to the known two isoforms, a new CNP isoform of MW 45 kDa was expressed in these cell lines and was the major type of isoform in F11 cells [24].
• Nonspecific association of 2',3'-cyclic nucleotide 3'-phosphodiesterase with the rat forebrain postsynaptic density fraction [24].
• Immunoblot analysis indicated that CNP is also expressed in neuronal stem cell lines, HiB5 and F11 [24].

Associations of Cnp1 with chemical compounds

• RESULTS: Immunohistochemistry revealed a decrease in the immature OL marker PLP on day 21 (P = .03) in LPS-exposed offspring, and an increase of the mature OL marker CNP on day 21 and at 8 weeks (P < .01, P < .001) [25].
• This was investigated by measuring cAMP production during the conversion of 32P-ATP to 32P-cAMP in the presence of an ATP regenerating system (30 micrograms creatine phosphokinase, 10 mM creatine phosphate), and the cyclic nucleotide phosphodiesterase inhibitor (1 mM IBMX) [26].
• This effect of FSH is preceded by a dose-dependent increase in intracellular cAMP, is potentiated by cyclic nucleotide phosphodiesterase inhibitors, and is mimicked by dibutyryl cAMP [27].
• Growth of muscle cells in the presence of agents that mimic cyclic AMP (cAMP) action or increase intracellular cAMP levels including 8-bromo-cyclic AMP (8-BrcAMP), cyclic nucleotide phosphodiesterase inhibitors, and forskolin increased sodium channel density up to 125% [28].
• Epinephrine or prostaglandin E1 caused a rise in the cyclic AMP content of normal cultures which was potentiated in the presence of the cyclic nucleotide phosphodiesterase inhibitor 1-methyl-3-isobutylxanthine or by forskolin, a diterpene activator of adenylate cyclase in intact cells [29].

Physical interactions of Cnp1

• Calmodulin coupled to Sepharose has provided a rapid and sensitive means of isolating a cyclic nucleotide phosphodiesterase activity which is stimulated by the calmodulin-Ca2+ complex, from rat parotid gland [30].

Co-localisations of Cnp1

• At the cellular level, JN in the rat CNS colocalized with 2',3'-cyclic nucleotide-3'-phosphodiesterase (CNPase), a cytoskeleton-related oligodendroglial protein [18].

Regulatory relationships of Cnp1

• 2) Insulin stimulated the expression of CNPase and G3PDH in culture [31].
• We measured the CNPase activities in the visual pathway tissues of Lewis strain rats with experimental allergic encephalomyelitis (EAE) induced by inoculation of myelin basic protein from the brain [32].

Other interactions of Cnp1

• At postnatal day 5-6 (P5-P6), the first CNPase(+) profiles appeared in the dorsal lateral olfactory tract adjacent to the accessory OB (AOB), followed by rare cell bodies and processes in AOB internal plexiform layer at P7 [22].
• The CNP-positive punctae were distributed throughout soma and dendrites, and distinct from PSD95-positive ones [24].
• The action of arginine vasopressin was mimicked by rolipram, an inhibitor of cyclic nucleotide phosphodiesterase type 4 [33].
• Treatment of brain-tissue slices with aTf produced a marked increase in the expression of MBP, CNPase, and tubulin mRNAs [34].
• In the presence of the cyclic nucleotide phosphodiesterase (PDE) inhibitor, 3-isobutyl-1-methylxanthine (IBMX), FSH-dependent cAMP accumulation was not affected by HGF [35].

Analytical, diagnostic and therapeutic context of Cnp1

• Molecular cloning and characterization of rat brain 2',3'-cyclic nucleotide 3'-phosphodiesterase isoform 2 [36].
• In situ hybridization revealed a thin longitudinal column of CNP-positive cells in the ventral ventricular zone of the embryonic day 14 rat spinal cord, coincident in time and space with cells that express the platelet-derived growth factor alpha receptor, another putative marker of the oligodendrocyte lineage [37].
• We have resolved multiple forms of cyclic nucleotide phosphodiesterase (PDE) in whole rat ventricle and in isolated rat ventricular myocytes by use of anion-exchange high-performance liquid chromatography [38].
• Radioimmunoassays for MBP and MAG and enzyme assays for CNP in whole homogenates of the aggregates revealed that each of these components increased with the progression of myelination [39].
• Peptide mapping of multiple forms of cyclic nucleotide phosphodiesterase [40].

References