Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.30.2 (endonuclease)
 18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Addition of extract of interferon (IFN)-treated HeLa cells to transcription reactions containing activated reovirion cores decreases the yield of viral mRNA (C. Baglioni, A. De Benedetti, and G. J. Williams, 1984, J. Virol. 52, 865-871). The 2'5'-oligo(A) (2-5A)-dependent endonuclease (RNase L) cleaves specifically viral mRNA, but little 5'-triphosphate 2-5A is recovered from these reactions by DEAE-cellulose chromatography. However, in the present study we detected microM concentrations of 2-5A derivatives by binding to RNase L. Similar results were obtained when the synthetic double-stranded RNA poly(I) X poly(C) was incubated with extract from IFN-treated cells: microM concentrations of 2-5A were detected by the binding assay, but little rRNA was degraded by RNase L. 2-5A derivatives which inhibited the activation of RNase L by authentic 2-5A were eluted from DEAE-cellulose with 90 mM KCl. These inhibitors were also formed by incubating purified 2-5A with HeLa cell extract. These results indicated that 2-5A was synthesized in the incubations with reovirion cores or poly(I) X poly(C), but that it was in large part degraded to compounds inhibitory for RNase L. IFN-treated HeLa cells were incubated with poly(I X C), but little rRNA degradation was detected in spite of the presence of high concentrations of 2-5A in these cells. Most of this 2-5A was eluted with 90 mM KCl from DEAE-cellulose and was inhibitory for RNase L. This indicated that 2-5A was degraded to inhibitory derivatives also in intact cells. The structure of the degradation products of 2-5A has not been established, but they contain free terminal phosphate(s), since their binding to RNase L and the inhibition of this enzyme is abolished by digestion with phosphatase.
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PMID:Inhibition of 2',5'-oligo(A)-dependent endoribonuclease by 2',5'-oligo(A) degradation products. 242 11

The synthesis and steady state level of immediate early vaccinia virus-specific RNAs in interferon-treated chick embryo fibroblasts were determined by blot hybridization analysis using the cloned restriction endonuclease fragment pEJ 18 containing the gene of vaccinia virus WR-specific DNA polymerase as a probe. Even though early vaccinia virus WR RNA was still synthesized, accumulation of immediate early viral RNAs was strongly inhibited. Accumulation of beta-actin RNA was not affected. This indicated an enhanced degradation of vaccinia virus WR-specific early RNAs in interferon-treated chick embryo fibroblasts. This notion was supported by Northern blot analysis which revealed degradation of residual RNA of vaccinia virus WR-specific DNA polymerase. In contrast to interferon-treated mouse L 929 cells, ribosomal RNA is not degraded in interferon-treated vaccinia WR-infected chick embryo fibroblasts.
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PMID:Increased turnover of vaccinia virus-specific immediate early RNAs in interferon-treated chick embryo fibroblasts. 244 63

A series of clones has been derived from an interferon-resistant murine cell line, Ltk- aprt-, and their antiviral properties have been characterized. In the parental Ltk- aprt- line interferon is unable to establish antiviral properties or to increase the levels of 2,5-oligo(A) synthetase, the 2,5-oligo(A)-activated endonuclease F, 2',5'-phosphodiesterase, or eIF-2 kinase. However, interferon did prevent replication of vesicular stomatitis, Mengo virus, and reovirus in some of the derivative cell lines. The effect of interferon on the levels of the enzymes of the 2,5-oligo(A) and eIF-2 kinase pathways did not correlate directly with the antiviral properties of these cell clones. Greatly increased levels of 2,5-oligo(A) synthetase occurred in one clone without activation of an antiviral state. Another clone exhibited antiviral activity without detectably increased 2,5-oligo(A) synthetase activity. Changes in the levels of endonuclease F and 2',5'-phosphodiesterase were slight in all the clones examined. Neither 2,5-oligo(A) synthetase nor eIF-2 kinase levels were altered by interferon in another clone and yet an antiviral state was established and prevented replication of vesicular stomatitis, Mengo virus, and reovirus. The results show that mechanisms other than the 2,5-oligo(A) and eIF-2 kinase pathways are likely to contribute to the antiviral effects of interferon.
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PMID:Induction of an antiviral state by interferon in the absence of elevated levels of 2,5-oligo(A) synthetase and eIF-2 kinase. 244

The interaction of herpes simplex virus type 1 (HSV-1) with murine macrophage cell lines was examined. The cell lines appeared to be moderately permissive for HSV-1 replication, though the yield of the virus was limited compared with that in Vero cells. Furthermore, the murine macrophage cell line SL-1, bearing Ia antigen, was persistently infected with HSV-1 for over one year, and was designated SL-1/KOS. Persistent infection could not be established in an Ia antigen-negative macrophage cell line, SL-4. In the SL-1/KOS culture, there was a small number of infected cells as revealed by infectious center assay. Treatment with monoclonal antibody against HSV-1 cured the persistent infection. Therefore maintenance of the persistent infection is considered to be due to a carrier culture consisting of a minority of infected cells and a majority of uninfected cells. In the SL-1/KOS cultures a low level of interferon (IFN) was found. When a large amount of exogenous recombinant murine IFN-beta (10(5)-10(6) international units/ml) was added to the culture, virus production diminished to undetectable levels. These results suggest that IFN plays an important role in the maintenance of persistent infection. In long-term persistently infected cultures, syncytium formation appeared and the virus from such cultures had a different DNA structure from that of the virus originally used for infection as revealed by restriction endonuclease analysis.
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PMID:Persistent infection with herpes simplex virus type 1 in an Ia antigen-positive murine macrophage cell line. 283 54

Phosphorylation of the alpha subunit of eukaryotic initiation factor 2 (eIF-2) causes mRNA to accumulate in 48 S complexes containing Met-tRNAf and eIF-2(alpha P). When the eIF-2 alpha kinase is inhibited by 2-aminopurine, the mRNA is slowly transferred from 48 to 80 S initiation complexes after an initial lag. The cause of this lag was examined by investigating whether mRNA and Met-tRNAf dissociated from 48 S complexes before binding to 80 S. Both compounds were quantitatively transferred from 48 to 80 S complexes after addition of 2-aminopurine and the eIF-2(alpha P) bound to 48 S complexes was dephosphorylated after an initial lag more slowly than unbound eIF-2(alpha P), which was rapidly dephosphorylated. the eIF-2(alpha P) in isolated 48 S complexes was slowly dephosphorylated by partially purified lysate phosphatases, whereas free eIF-2(alpha P) was readily dephosphorylated. These results indicated that 48 S complexes could directly join to a 60 S ribosomal subunit after eIF-2(alpha P) dephosphorylation. The lag and slow kinetics of dephosphorylation of eIF-2(alpha P) bound to 48 S complexes accounted for the slow transfer of mRNA from 48 to 80 S complexes. Moreover, the mRNA bound to 48 S complexes was more susceptible to cleavage by an endonuclease than mRNA in polyribosomes, as shown by activating the (2'-5')oligo(A)-dependent endonuclease. This finding is discussed in view of the possible role of eIF-2 alpha kinase and endonuclease in the inhibition of viral mRNA translation in interferon-treated cells.
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PMID:Kinetics of dephosphorylation of eIF-2(alpha P) and reutilization of mRNA. 298 50

Human papillomavirus type 6 (HPV-6) DNA was detected in a rapidly growing vulvar verrucous carcinoma and two recurrent tumor samples. The viral DNA (HPV-6vc) was molecularly cloned and found to have a high degree of DNA sequence homology to HPV-6b DNA. Comparison of restriction endonuclease cleavage patterns between HPV-6b and HPV-6vc genomes and DNA sequencing analysis demonstrated an additional 106 bases in the HPV-6vc genome. These additional nucleotides were located in the noncoding region of the viral genome which contains the putative viral DNA replication and early gene transcriptional control elements. Seventy-four of the additional 106 nucleotides were found as one insert in the purine-thymidine-rich region 3' to the end of the L1 open reading frame. This 74-base-pair addition had homology with viral sequences immediately upstream to it and to poly(dG-dT) sequences found in the human genome including the conserved repeated sequences in human DNA (EC1) and in the human cardiac muscle actin gene. Two smaller inserts, 19 and 15 nucleotides, were found upstream from the transcriptional control elements and demonstrate homology with regions of human alpha and gamma interferon genes.
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PMID:Isolation and characterization of a novel human papillomavirus type 6 DNA from an invasive vulvar carcinoma. 300 57

HeLa cells generally do not respond well to interferon (IFN). We have used is-1, an IFN-sensitive mutant of mengovirus, to select a clone of IFN-responsive HeLa cells (F-H12). At moderate levels of human alpha/beta IFN, is-1 yields were fivefold lower in these cells than in similarly protected control cells. In contrast, wild-type mengovirus, vesicular stomatitis virus and a wild-type and thymidine kinase-negative strains of herpes simplex virus type 1 grew equally well in both cell lines. By a cell survival assay, the F-H12 line was up to 100 times more responsive to IFN than the parental line when challenged by is-1. 2'-5'-Oligo(A)-dependent endonuclease activity was the same in both lines. These observations cannot be accounted for by enhanced induction of IFN following infection.
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PMID:Selection and characterization of an interferon-responsive clonal cell line of HeLa cells. 302 28

A brief exposure (for 6 h) of U937 cells to interferon (IFN)-gamma (500 U/ml) followed by a long term incubation of cells in normal medium for 8 or more weeks resulted in the induction of cells that were refractory to the anticellular and differentiating effects of not only IFN-gamma but also IFN-alpha and IFN-beta at concentrations up to 10(4) U/ml. In addition, the cells became insensitive to the potent differentiating effect of the phorbol ester--tumor promoting agent (TPA). However, the resistant cells retained their sensitivity to the antiviral effect of different IFNs and were fullu responsive to the induction of endonuclease 2',5'-oligoadenylate (2-5A) synthetase by IFN. Furthermore, the resistant cell population appeared to be homogeneous because clones derived from single cells from this population all exhibited the same resistant phenotype to IFN and TPA. These results suggest that induction of resistant U937 cells may involve a dedifferentiation process which results in the formation of an immature cell population that do not respond to the differentiating and/or anticellular effects of various types of IFNs.
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PMID:Biological characteristics of interferon-r-induced resistant histiocytic lymphoma cell line U937. 311 22

The levels of a (2'-5')An-dependent endonuclease (RNase L) were determined in extracts prepared from murine L cells and Ehrlich ascites tumor (EAT) cells by measuring specific binding of protein to a labeled derivative of (2'-5')An, (2'-5')A3[32P]pCp. RNase L levels were found to depend both on interferon (IFN) treatment and on cell growth conditions. Treatment of murine L cells and EAT cells with 100-2,000 IRU IFN beta or IFN gamma resulted in a similar 2-4-fold increase in the levels of RNase L when cells were present at low density. The levels of RNase L were also shown to increase 2-3-fold as cells approached saturation density. Serum-starved cells also displayed relatively high levels of RNase L. RNase L levels in cells maintained at high cell density did not change appreciably following treatment with IFN beta or IFN gamma. Regulation of RNase L levels by cell growth conditions as well as by IFN beta or IFN gamma treatment suggests that RNase L may play an important role in regulating the levels of cellular mRNAs as well as acting to degrade viral RNAs.
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PMID:(2'-5')An-dependent endoribonuclease: enzyme levels are regulated by IFN beta, IFN gamma, and cell culture conditions. 314 77

La Crosse virus infection of BHK cells leads to a dramatic shutoff of not only host protein synthesis but also viral protein synthesis later in infection. This shutoff can be accounted for by the loss of the cytoplasmic cellular and viral mRNAs. The induction of mRNA instability requires extensive virus replication, since when cycloheximide is added early in infection the preexisting viral and cellular mRNAs do not decrease upon incubation of the cultures. Pretreatment of the cultures with actinomycin D does not affect the ability of La Crosse virus infection to induce mRNA instability, and examination of the rRNAs shows no evidence of specific degradation due to activation of the interferon-associated latent RNase. The induction of mRNA instability therefore does not appear to operate through an interferon pathway. Viral mRNA synthesis, on the other hand, is not turned off during infection, and the cap-dependent endonuclease involved in viral mRNA initiation may be responsible for the mRNA instability.
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PMID:La Crosse virus infection of mammalian cells induces mRNA instability. 333 45


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