Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.27.1 (RNase)
 16,360 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bovine seminal ribonuclease (BS-RNase), a dimeric homologue of RNase A, cleaves both single- and double-stranded RNA and inhibits the growth of tumor cells. Its catalytic activity against double-stranded RNA, either homopolymeric ([3H]polyA/polyU) or mixed sequence, is enhanced by bovine or human recombinant interferon-gamma (IFN-gamma). Activation is seen with as little as 4-10 interferon units per assay. Enhancing the degradation of double-stranded RNA, an intermediate in the growth cycle of many viruses, could contribute to IFN-gamma's ability to control cell growth and induce an antiviral state.
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PMID:Interferon-gamma activates the cleavage of double-stranded RNA by bovine seminal ribonuclease. 212 24

2',5'-oligoadenylates known as 2-5A [px(A2'p)nA; chi = 2 or 3, n greater than or equal to 2] are produced in interferon-treated cells in response to double-stranded RNA. 2-5A binds with high affinity to a 2-5A-dependent RNase resulting in the cleavage of single-stranded RNA. An efficient, rapid, and extremely sensitive photoaffinity labeling method was developed to facilitate detection of 2-5A-dependent RNase. A bromine-substituted and radioactive derivative of 2-5A, the 5'-monophosphate, p(A2'p)2(br8A2'p)2A3'-[32P]Cp, was synthesized as probe for 2-5A-dependent RNase. Even though this bromine-substituted analog of 2-5A bore no 5'-terminal triphosphate or diphosphate, it bound to 2-5A-dependent RNase with the same high affinity as did 2-5A per se but it was a less effective activator of the RNase under the present assay conditions. The presence of bromine atoms in the 2-5A analog enhanced by more than 200-fold crosslinking to 2-5A-dependent RNase under a uv lamp; many additional polypeptides were also labeled but at much lower levels. Furthermore, using high-intensity uv laser irradiation (308 nm) covalent attachment of the bromine-substituted 2-5A analog to 2-5A-dependent RNase was readily achieved within 10(-6) s.
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PMID:Photochemical crosslinking in oligonucleotide-protein complexes between a bromine-substituted 2-5A analog and 2-5A-dependent RNase by ultraviolet lamp or laser. 232 73

Alkaline ribonuclease (RNase; EC 3.1.27.5) activities and 2',5'-oligoadenylate synthetase (2-5 AS; no EC no. assigned) activities in serum were measured in nine patients with hepatitis B e antigen-positive chronic hepatitis B before, during, and after treatment with recombinant human interferon alpha-2b for four weeks at daily doses ranging from 3 to 10 mega-units. Alkaline RNase activities in serum significantly increased from 65.8 +/- 9.5 units/L (mean +/- SD) to 84.3 +/- 11.9 units/L after the first week of therapy (P less than 0.001). (One unit of RNase activity is defined as that increasing the absorbance at 260 nm by 1.0 in 1 min). This increase persisted during and until two weeks after the end of the therapy, at which time the mean RNase activity in serum was still significantly increased (70.8 +/- 9.4 units/L, P less than 0.01). Before therapy, phosphocellulose chromatography of RNase showed five active peaks of enzyme activity, which were similar to that observed even when RNase activity increased immediately after therapy. There was a close correlation between RNase activities and the logarithm of 2-5 AS activities, measured simultaneously in each patient. We conclude that recombinant alpha-interferon therapy increases RNase activities in serum, associated with the increased 2-5 AS activities.
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PMID:Effects of recombinant leukocyte interferon on ribonuclease activities in serum in chronic hepatitis B. 235 34

The possibility of generating large quantities of highly active interferon from human placenta amniotic membrane (plaferon) has been demonstrated. Plaferon is innocuous and nonreactogenic in experimental models and has an antiviral effect of wide spectrum. The activity is resistant to DNase, RNase, lipase, and stable at pH 2. A polyclonal serum to human leukocyte interferon and monoclonal NK-2 antibody did not inhibit the antiviral activity of plaferon. The level of hormones in plaferon and leukocyte interferon preparations was practically similar. In diploid cultures of human fibroblasts the antiviral condition under the effect of plaferon developed slower than under the effect of leukocyte interferon.
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PMID:[Physicochemical and biological properties of human placental amniotic interferon]. 242 70

Previously we have shown that inhibition of replication of vesicular stomatitis virus in interferon-treated JLSV-11 cells is at least partly caused by impaired viral primary transcription. Here we report that subviral particles isolated from interferon-treated infected cells were deficient in mRNA synthesis in vitro compared with the particles isolated from untreated cells. This was due to the presence of an associated ribonuclease activity which hydrolyzed not only newly synthesized viral mRNAs but also exogenously added viral transcripts.
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PMID:Ribonuclease activity is associated with subviral particles isolated from interferon-treated vesicular stomatitis virus-infected cells. 244 94

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


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