Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.27.5 (RNase)
 17,967 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A nucleic acid-rich fraction extracted and purified from BCG (MY-1) augmented natural killer (NK) cell activity of mouse spleen cells in vitro, and produced factor(s) which showed anti-viral activity and rendered normal macrophages cytotoxic towards tumor cells. These cellular responses were induced by the MY-1 digested preliminarily with RNase, but not by the MY-1 digested with DNase, indicating that DNA contained in MY-1 was essential for the responses. The function of the factor to activate macrophages was destroyed by treatment with a small amount of anti-interferon (IFN)-gamma antiserum or under acidic conditions (pH 2), but not by treatment with anti-IFN-alpha/beta antiserum, while the anti-viral activity was destroyed almost completely by treatment with anti-IFN-alpha/beta antiserum. It appears that DNA from BCG stimulated mouse spleen cells in vitro, resulting in augmentation of NK activity and production of IFN-alpha/beta and -gamma.
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PMID:In vitro augmentation of natural killer cell activity and production of interferon-alpha/beta and -gamma with deoxyribonucleic acid fraction from Mycobacterium bovis BCG. 245 94

Alterations in the morphology and histochemistry of vascular endothelial cells (EC) have been repeatedly observed at sites of chronic inflammation and immune reactions. These changes, which are most prominent in the EC postcapillary venules present in areas with large lymphocytic infiltrates, include the acquisition of a columnar or cuboidal morphology, the development of ribonuclease-sensitive metachromasia, and an increase in intracellular organelles. Thus, EC at sites of inflammation appear to be activated and to demonstrate increased metabolic activity. This study reports that both tumor necrosis factor-alpha (TNF) and lymphotoxin (LT) can activate cultured human umbilical vein EC, as measured by: 1) increased adhesiveness for lymphocytes, 2) increased cell metabolism, as measured by RNA and protein synthesis, and 3) increased cell volume. Although gamma interferon (IFN-gamma) and interleukin-1 (IL-1) have been shown previously to stimulate EC adhesiveness for lymphocytes, these two cytokines had only marginal effects on EC RNA and protein synthesis, and both caused a decrease in EC volume. These findings suggest that TNF and LT play a role in the type of activation of EC in vivo that leads to the development of tall endothelium and increased lymphocyte emigration.
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PMID:Endothelial cell activation induced by tumor necrosis factor and lymphotoxin. 246 2

Double-stranded (ds) RNA and many viruses are inducers of interferon (IFN), the latter presumably because they contain, or can form, dsRNA. Concomitant with the induction of IFN in chicken embryo cells was the induction of a novel double-stranded ribonuclease (dsRNase), which was released into the medium and continued to accumulate long after IFN production ceased. Only avian cells (chicken, quail, turkey, or duck) expressed high levels of this dsRNase; mammalian, turtle, or fish cells did not. Production of the nuclease was inducer dose-dependent. Optimum pH and cation requirements distinguished it from other dsRNase activities. Degradation of dsRNA was endonucleolytic. Activity resided in a molecule of an Mr of approximately 34,500. Low levels of a single-stranded (ss) RNase activity were inseparable from the dsRNase. The role for a dsRNA-inducible dsRNase released from cells is unknown.
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PMID:Double-stranded ribonuclease coinduced with interferon. 247 Dec 68

In this study we have examined if resistance of vaccinia virus to interferon (IFN) correlates with virus-induced alterations of the 2-5A system. We have shown that in various IFN-treated vaccinia virus infected cells of mouse, monkey and human origins, the intracellular levels of 2-5A are low early in infection but exhibit a sharp rise late in infection. In spite of the presence of 2-5A, activation of the 2-5A dependent RNase, as measured by the rRNA cleavage assay, does not occur or is delayed in the course of virus infection. However, when cycloheximide, an inhibitor of protein synthesis is added at the time of virus infection, extensive cleavage or rRNA is observed in IFN-treated, infected cells. If cycloheximide is added at various times after virus infection, rRNA cleavage is gradually prevented and a virus-induced inhibitor of the 2-5A system can be detected between 1-2 hr post infection. A function encoded by a ts 22 mutant of vaccinia virus blocked rRNA cleavage. Restriction of rRNA cleavage during virus infection correlated with dephosphorylation of 2-5A. Our findings suggest that modulation of the 2-5A system by vaccinia virus involves the production of an activator and simultaneous synthesis of an inhibitor(s). Viral ds-RNA is likely to be the activator while a function encoded by ts 22 mutant is involved in inhibition of the 2-5A system. Other viral functions (ATPase and phosphatase) may also be involved in modifications of the 2-5A system by regulating 2-5A levels and altering the integrity of 2-5A. Modifications of the 2-5A system, during vaccinia virus infection might contribute to the resistance of this cytoplasmic DNA virus to IFN.
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PMID:Resistance of vaccinia virus to interferons: modulation of the 2-5A system in interferon-treated, vaccinia virus infected cells. 247 64

The effect of immunizing healthy individuals with either tetanus toxoid or yellow fever live attenuated vaccine was examined by measuring interferon (IFN)-dependent oligoadenylate synthetase (2-5A) activity. This enzyme converts ATP into oligonucleotides coupled together in 2'-5'diester bonds. The synthetized products possess among other effects growth inhibiting properties and stimulate a latent RNase, thus playing an important role in the defense against viral infections. Although 2-5A activity is known to increase following virus infections and perhaps therefore to reflect a previous IFN exposure, little is known about the ability of vaccines to activate 2-5A in healthy individuals. Controlled dosages of commercially available vaccine preparations were therefore administered to 17 healthy Danish volunteers. In one study, the effect of a primary stimulus, yellow fever, was tested. It was found that the 2-5A activity increased to reach a peak by 1,000% by day nine. In another study, the effect of a secondary stimulus or booster, Tetanus toxoid, was tested. The response to this antigen was a 40% decrease in 2-5A activity from day 1 to day 18. Thus, the 2-5A activity highly reflects the type of antigen used for immunization and possibly even whether the individuals previously had been exposed to the given antigen. As IFNs are very shortlived in vivo measuring 2-5A activity is a sensitive way of estimating changes in blood immune cells to exogenous antigens.
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PMID:Postimmunization activity of oligoadenylate synthetase in peripheral blood lymphocytes from healthy individuals. 248 11

(2'-5')An-dependent RNase functions as a translational regulatory protein which mediates interferon action. Levels of this enzyme are decreased in barrier-reared Balb/c (+/+), Balb/c (+/nu), and Balb/c (nu/nu) mice when compared to conventionally reared Balb/c (+/+) mice. This suggests that high levels of (2'-5')An-dependent RNase in conventionally reared mice are maintained by continuous exposure to microbial flora which may induce interferons. Interferon treatment of barrier-reared mice does not, however, result in an increase in (2'-5')An-dependent RNase levels. This suggests that responsiveness to interferons is decreased in barrier-reared mice. The high levels of (2'-5')An-dependent RNase which are maintained in normal mice under physiological conditions may be important for rapid and effective defense against viral pathogens.
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PMID:(2'-5')An-dependent RNase: enzyme levels are decreased in barrier-reared control and IFN-beta or IFN-gamma treated Balb/c mice. 251 62

The intracellular effector oligonucleotides ppp(A2'p)nA (n = 2- greater than or equal to 4) regulate the breakdown of RNA by activating ppp(A2'p)nA-dependent RNase. Cellular levels of this RNase were demonstrated to be regulated during differentiation of murine embryonal carcinoma cells. An induction of this RNase by interferon was demonstrated in each of three differentiated cell types (F9 clone 9, PYS, and PSA 5E) by analyzing rRNA breakdown following the introduction of ppp(A2'p)nA into the intact cells. In contrast, in three undifferentiated embryonal carcinoma cell lines (F9, PC13 clone 5, and Nulli 2A) there was little if any ppp(A2'p)nA-dependent RNase either with or without interferon pretreatment. These results were confirmed by affinity labeling of the RNase in cell-free systems. Addition of the proteinase inhibitor, leupeptin, to the cell lysis buffer was necessary to stabilize the RNase against cleavage to discrete breakdown products. Moreover, during differentiation of PC13 clone 5 cells by retinoic acid and N6,O2'-dibutyryl-adenosine 3',5'-monophosphate there was a gradual induction of ppp(A2'p)nA-dependent RNase. The expression of this RNase is, therefore, greatly enhanced during cell differentiation. In addition, the double-stranded-RNA-dependent protein kinase was investigated and was found to be interferon-inducible in all of the cell lines regardless of the state of cell differentiation.
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PMID:Regulation of ppp(A2'p)nA-dependent RNase levels during interferon treatment and cell differentiation. 257 57

Murine embryonal carcinoma F9 cells, a tissue culture model for early embryonic development, do not produce interferon (IFN) in response to poly(I-C), as determined by an antiviral assay. RNase protection analyses were used to examine total RNA extracted from the cells for the presence of beta-IFN RNA. Whereas F9 cells differentiated in vitro with retinoic acid produced a biologically active protein as well as beta-IFN RNA in response to poly(I-C), undifferentiated F9 cells produced no detectable beta-IFN RNA even in the presence of cycloheximide, an IFN-superinducing agent. These results show that undifferentiated embryonal carcinoma cells do not accumulate beta-IFN RNA in response to an IFN-inducing agent, suggesting a transcriptional regulatory mechanism. However, this control mechanism is altered upon differentiation, since the gene can be transcriptionally activated in retinoic acid-differentiated cells.
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PMID:Control of beta-interferon expression in murine embryonal carcinoma F9 cells. 279 97

The expression of the gene for the murine tissue inhibitor of metalloproteinases (TIMP) is induced in response to viruses, growth factors, and phorbol esters. In this report we show that the accumulation of TIMP mRNA after Newcastle disease virus induction is caused by transcriptional activation of the gene. Comparison of the sequences of cDNA and genomic clones along with RNase protection and primer extension analyses revealed that the murine TIMP gene possesses multiple cap sites and that the exon 1 consists exclusively of 5'-noncoding sequences. We observed that DNA regions analogous to those found upstream of the virus-inducible interferon genes are present within intron 1 of the TIMP gene. To investigate the possible role of TIMP intron 1 in gene expression, we used a functional assay based on the transfection of plasmids in which the DNA segment to be tested is placed in proximity to a marker gene driven by the heterologous herpes simplex virus thymidine kinase promoter. Our results indicate that TIMP intron 1 contains DNA sequence elements capable of modulating the activity of a heterologous promoter in two different ways: (i) by enhancing constitutive expression and (ii) by conferring virus inducibility. These results suggest that intron 1 may be involved in the transcriptional regulation of TIMP gene expression.
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PMID:Presence of transcription regulatory elements within an intron of the virus-inducible murine TIMP gene. 285 Apr 84

Activation of the ppp(A2'p)nA (2-5A)-dependent RNase was investigated during the abortive infection of BSC40 cells by a temperature-sensitive mutant of vaccinia virus, ts22. At the nonpermissive temperature, ts22 has an abortive late phenotype. At the onset of late-viral-gene expression, viral mRNA is degraded and rRNA is cleaved into discrete fragments in the absence of prior interferon treatment (R. F. Pacha and R. C. Condit, J. Virol. 56:395-403, 1985). Concomitant with rRNA cleavage, an increase in 2-5A occurred late during infection. Discrete 18S- and 28S-rRNA degradation products from BSC40 cells infected with ts22 at the nonpermissive temperature comigrated in denaturing agarose gels with rRNA cleaved fragments produced by the activation of 2-5A-dependent RNase in uninfected cells transfected with exogenous 2-5A. An increase in 2-5A levels and a similar discrete and characteristic degradation of rRNA were observed in BSC40 cells infected with wild-type vaccinia virus in the presence of isatin-beta-thiosemicarbazone. The results show that the ts22 lesion and the action of isatin-beta-thiosemicarbazone may affect the same pathway, leading to the activation of latent 2-5A-dependent RNase and resulting in indiscriminate RNA degradation and inhibition of viral replication.
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PMID:Modulation of ppp(A2'p)nA-dependent RNase by a temperature-sensitive mutant of vaccinia virus. 291 Nov 26


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