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

Foot-and-mouth disease virus (a member of the picornavirus group) RNA could be translated effectively in an S-30 extract from Ehrlich ascites tumour cells. This translation was inhibited by aurintricarboxylic acid, cycloheximide, puromycin and RNase. Cell-free products of translation were identified by disc gel electrophoresis and immunoprecipitation with specific antisera. Gel electrophoresis of the products without prior immunoprecipitation suggested the synthesis of some of the non-capsid proteins and capsid proteins VP1, VP2 and VP3 of the virus. Immunoprecipitations with antisera against whole virus and VP3 indicated the synthesis of VP3 and of at least two additional peptides of 100 000 and 56 000 daltons containing antigenic sites of VP3. Gel electrophoresis after immunoprecipitation with antiserum against virus infection-associated antigen indicated the synthesis of a different 56 000-dalton protein appearing to resemble non-capsid protein NCVP5. The amount of foot-and-mouth disease virus and VP3-specific peptides in the virus RNA-directed products were measured by immunoprecipitation.
J Gen Virol 1976 Sep
PMID:Cell-free translation of foot-and-mouth disease virus RNA into identifiable non-capsid and capsid proteins. 6 Dec 50

C-type particles secreted in vivo by MOPC-315 myeloma cells were characterized. These particles localize at a density of 1-16 g/ml in sucrose and possess a 60 to 70S RNA and an RNA-instructed DNA polymerase. Endogenous enzyme activity requires manganese and is inhibited by ribonuclease or by the omission of any of the deoxynucleoside triphosphates. The enzyme utilizes the virus 60 to 70S RNA as a template to synthesize DNA molecules which specifically hybridize to the homologous RNA.
J Gen Virol 1976 Aug
PMID:RNA-instructed DNA polymerase associated with C-type particles produced in vivo by murine myeloma cells. 6 43

Purified preparations of L cell virions (LCV) were found to possess an associated DNA polymerase activity. This enzyme was active with poly(C).oligo(dG) and poly(Cm).oligo(dG) and was able to transcribe poly(A).oligo(dT). Endogenous DNA synthesis was also demonstrable in disrupted virion preparations but this reaction was enhanced, rather than inhibited, by RNase pre-treatment. The effects of variations in a number of the assay parameters on these activities were examined in an attempt to determine the class of DNA polymerase involved.
J Gen Virol 1979 Mar
PMID:Demonstration of an unusual DNA polymerase activity associated with the L cell virion. 8 90

Although poly(I) is generally considered to be inactive as an interferon inducer, we have found several authentic poly(I) preparations to be effective inducers. Their interferon inducing ability varied considerably from one cell system to another. In human diploid fibroblasts, primed with interferon and superinduced by cycloheximide and actinomycin D, all active poly(I) samples proved nearly as effective in inducing interferon as poly(I).poly(C). In primary rabbit kidney cell cultures, the active poly(I) samples were either as active, or 3 to 30 times less active than poly(I).poly(C). In intact rabbits they were 100 times less active than poly(I).poly(C). Except for one particular sample, all active poly(I) preparations were inferior to poly(I).poly(C) when assayed for interferon induction in interferon-treated mouse L cells; in DEAE-dextran-treated L cells, they induced little, if any, interferon. The poly(I) inducers of interferon were considerably more susceptible to degradation by TI ribonuclease, pancreatic ribonuclease and human serum nuclease(s) than was poly(I).poly(C) when assayed under the same conditions. Due to their limited half-life time in biological fluids, poly(I) analogues such as those described here may offer a greater safety margin in clinical use than poly(I).poly(C).
J Gen Virol 1978 Jul
PMID:Interferon inducing activity of polyinosinic acid. 9 86

The envelope spikes of Sindbis and Semliki Forest virus are arranged in a T = 4 icosahedral surface lattice and, by deduction, it has been suggested that the nucleocapsid proteins are similarly arranged. After treatment of the virions with a non-ionic detergent the released nucleocapsids sediment in sucrose gradients at about 160S and 150S and have densities in CsCl of 1.42 g/ml and 1.425 g/ml, respectively, for Sindbis and Semliki Forest virus. At pH 6.0 Sindbis nucleocapsids do not contract like those of Semliki Forest virus. Nucleocapsids of both viruses are sensitive to the action of ribonuclease but only those of Semliki Forest virus undergo a drastic structural rearrangement due to the treatment. EDTA treatment in hypotonic conditions results in a decrease in the S-value for both particles. Electron micrographs show that the SFV nucleocapsids are partly 'unfolded' while those of Sindbis appear slightly contracted after exposure to EDTA.
J Gen Virol 1979 Oct
PMID:Comparison of the structural properties of Sindbis and Semliki forest virus nucleocapsids. 11 37

Infectious bovine rhinotracheitis (IBR) virus was grown in the presence of 5-3H-uridine in a continuous line of bovine kidney cells. 5-3H-uridine was found to be associated with viral nucleocapsids. Furthermore, purification of the viral nucleic acid present in nucleocapsids illustrated that 5-3H-uridine was part of the viral nucleic acid. Purification of viral DNA from infected cells also indicated that 5-3H-uridine was associated with viral nucleic acid possibly as ribonucleotides. The label was identified as RNA by measuring its susceptibility to RNase and analysis of the bases. Short pulses with 5-3H-uridine, resulted in labelled nucleic acid which was extremely sensitive to RNase and alkali but resistant to DNase. Nucleotide analysis indicated that after short pulses all the radioactivity was associated with the base uracil whereas upon longer labelling periods a large percentage of the label was associated with cytosine. However even if viral DNA was isolated from nucleocapsids there was still some radioactivity associated with uracil. Sedimentation of heat denatured 5-3H-uridine label viral nucleic acid in CS2SO4 indicated that the label sedimented at a density of single stranded DNA suggesting that the ribonucleotides are covalently linked to the viral DNA.
J Gen Virol 1976 May
PMID:Ribonucleotides in infectious bovine rhinotracheitis virus DNA. 18 Feb 41

Primary human amnion cell monolayers which had been treated with DEAE-dextran, washed, and then inoculated with sonicated cells of the EB3 line of Burkitt's lymphoma cells developed foci of transformed amnion cells 7 to 14 days later. When either the DEAE-dextran or the sonicate was omitted, no significant transformation was found. The foci consisted of enlarging mounds of rapidly dividing cells, which upon subculturing continued their high miotic activity; and strains or lines of the transformed amnion cells were thus readily established. The modal number of chromosomes in such lines was 65 instead of the normal 46. Not all human amnions yielded cells transformable by EB3 cell sonicate, as determined by direct comparisions using the same cultural conditions and testing with the same fresh sonicate preparation in the same experiment. Overall, it appeared that only about 40 to 50% of the amnions yielded transformable cell monolayers; the rest gave monolayers apprently completely refractory to the transformation. The transformed amnion cells contained nuclear and cytoplasmic Epstein-Barr virus (EBV) antigen(s), as revealed by indirect immunofluorescence tests. EB3 cell sonicate also caused the appearance of rapidly growing transformed cell foci on secondary rat embryo cell monolayers which had been sensitized with DEAE-dextran. Calcium in the cell maintenance medium decreased the number of transformed foci found, both on the human and on the rat cell monlayers. Sonicates of cultured normal human leucocytes had no such transforming activity for either the human or the rat cells. The transforming agent in EB3 cell sonicate was completely destructible by either deoxyribonuclease or trypsin, but not by ribonuclease, and was not neutralizable by anti-EBV serum. The simplest interpretation of these results is that the transforming agent is part of all of the EBV DNA plus some necessary protein, with both the DNA and the protein accessible to hydrolytic enzyme action.
J Gen Virol 1976 Jun
PMID:Use of a transfection method to demonstrate a monolayer cell transforming agent from the EB3 line of Burkitt's lymphoma cells. 18 Feb 48

Two newly synthesized pyrimidine derivatives were found to possess antiviral activity against Mengovirus in Fogh and Lund (FL) cells and in a cell-free system. The inhibitory effect on RNA-dependent RNA polymerase of Mengovirus-infected FL cells was assayed using 14C-UTP as precursor. Addition of 50 or 100 muM of the inhibitors in a cell-free system of crude enzyme and nucleoside triphosphate medium for 60 min incubation at 37 degrees C resulted in about 40 to 60% lower counting rates for drug-treated reaction mixtures. The analysis of the polymerase synthesis product (virus RNA extracted from the cell-free reaction mixture and deproteinized by the phenol-SDS method) was carried out by means of agarose-acrylamide gel electrophoresis. The main finding was a reduction of single-stranded Mengovirus RNA (RNase-sensitive and LiCl-precipitable). The rates of synthesis of the replicative intermediate (LiCl-precipitable) and the replicative form of RNA (LiCl-soluble) were not significantly influenced.
J Gen Virol 1977 Jan
PMID:Effects of pyrimidine derivatives on RNA-dependent RNA polymerase of mengovirus-infected Fogh and Lund (FL) cells. 18 80

Complementary single-stranded RNAs from three independent VSV defective interfering particle (DI) sources examined can anneal and give rise to monomeric and multimeric circular and linear double-stranded structures observable by electron microscopy under aqueous conditions. When the RNA from the shortest of these DI is spread from 80% formamide solutions, as many as 32% of the molecules are circular, suggesting that the single-stranded RNAs contain inverted complementary terminal sequences. This is strongly supported by the isolation of the putative terminal sequences which rapidly become RNase resistant base-paired structures after melting and quick-cooling the RNA. RNase digestion yields a major and a minor component, 60 to 70 and 135 to 170 nucleotides long respectively. Snap-back DI RNAs also contain inverted complementary sequences at both ends of the plus and minus strands of the duplexes since nicking these at the ends gives rise to double-stranded molecules which can form monomeric and multimeric circular and linear molecules. Thus, snap-back molecules most likely contain a covalent linkage between or near complementary terminal sequences on the two complementary strands as schematically shown in Fig. 5D.
J Gen Virol 1978 Jan
PMID:Inverted complementary terminal sequences in single-stranded RNAs and snap-back RNAs from vesicular stomatitis defective interfering particles. 20 71

Synthesis of cellular protein was substantially inhibited within 1 h of infection with herpes simplex virus, type 2, strain G (HSV-2). The inhibition also occurred, although no virus-specific protein synthesis was detected, after infection with u.v. irradiated virus and in cytoplasts that had been enucleated before infection. The inhibitory activity could not be distinguished from infectivity by dilution, sedimentation or reaction with gamma-globulin. HSV-2 also suppresssed the synthesis of Sendai virus proteins, but not those specified by HSV-1. Host protein synthesis was no more sensitive than virus protein synthesis to an increased concentration of NaCl in the medium, nor could the suppression of host synthesis be prevented by adding excess MgCl2 to the medium or by omitting CaCl2 or NaCl. It was accompanied by the breakdown of polyribosomes, which also occurred in the presence of cycloheximide but not at 4 degrees C. The breakdown yielded ribosomes that were sensitive to a high salt concentration, unlike those produced by treatment of polyribosomes with RNase. The synthesis of cellular DNA and RNA was also inhibited following infection with u.v.-inactivated virus. It is concluded that the suppression of host protein synthesis (and probably also of host DNA and RNA synthesis) is caused by a constituent of the infecting virus particles. The mechanism is obscure but probably does not depend on the leakage out of the cell of Mg2+ or into the cell or Ca2+ or Na+ ions, nor on the specific inhibition of initiation of host polypeptide chains, nor on RNase-like attack on host polyribosomes.
J Gen Virol 1978 Oct
PMID:Suppression of the synthesis of cellular macromolecules by herpes simplex virus. 21 20


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