Interferon-associated, dsRNA-dependent enzyme activities in a mutant 3T6 cell engaged in the semiconstitutive synthesis of interferon

Jarvis, Allan P.; White, Carol N.; Ball, A. P.; Gupta, Saloni; Ratner, Lee; Sen, Ganes C.; Colby, Clarence

doi:10.1016/0092-8674(78)90343-4

Cited by 25 publications

(8 citation statements)

References 15 publications

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“…PKR is induced in an inactive form by interferon and activated by binding to viral dsRNA, which causes dimerization and autophosphorylation (27)(28)(29). However, in the present study, exogenously expressed wild-type PKR could prevent protein translation (Fig.…”

Section: Discussioncontrasting

confidence: 49%

“…Double-stranded RNA (dsRNA)-activated protein kinase (PKR) phosphorylates the ␣-subunit of eukaryotic initiation factor 2 (eIF2␣) to inhibit cap-dependent translation (22)(23)(24)(25) and plays a role in the innate immune response to viral infection and several cellular signal transduction pathways (26). PKR is induced by interferon and activated by binding to dsRNA, which causes the homodimerization and autophosphorylation of the kinase (27)(28)(29). PKR is an anti-viral molecule that recognizes viral RNA and inhibits viral protein translation.…”

mentioning

confidence: 99%

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Activation of Double-stranded RNA-activated Protein Kinase (PKR) by Interferon-stimulated Gene 15 (ISG15) Modification Down-regulates Protein Translation

Okumura

Uematsu

et al. 2013

Journal of Biological Chemistry

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Background: Double-stranded RNA-activated protein kinase (PKR) is activated by virus-derived RNA and inhibits protein translation. Results: PKR is covalently modified by interferon-stimulated gene 15 (ISG15), and ISG15-PKR fusion protein is active without virus RNA. Conclusion: PKR is able to be activated by ISG15 modification. Significance: PKR might be an anti-tumor molecule by inhibiting protein translation in ISG15-positive cancer cells.

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Section: Discussioncontrasting

confidence: 49%

mentioning

confidence: 99%

Activation of Double-stranded RNA-activated Protein Kinase (PKR) by Interferon-stimulated Gene 15 (ISG15) Modification Down-regulates Protein Translation

Okumura

Uematsu

et al. 2013

Journal of Biological Chemistry

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“…In these cells viral growth was inhibited at variety of steps including adsorption [14,15,32], penetration [2,18,22,23,27,30,31,38], and intracellular transport or modification of viral proteins [1,9,31,33,[35][36][37]. Other mutant cell lines were producing interferons constitutively [t 1,12,24]. In most cases, however, mutant cell lines were only poorly characterized and host factors altered in those cells remain largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Isolation and characterization of a novel mutant mouse cell line resistant to Newcastle disease virus: constitutive interferon production and enhanced interferon sensitivity

Aoki

Ohhira

Hoshino

et al. 1994

Archives of Virology

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In our attempt to isolate mutant cell lines resistant to Newcastle disease virus (NDV) we developed an improved procedure for enrichment of NDV-resistant cells from mouse FM3A cells and isolated a novel NDV-resistant mutant cell line, Had-2, with characteristics different from Had-1, a previously reported NDV-receptor-deficient mutant strain. Had-2 cells adsorbed NDV normally but the accumulation of viral mRNAs and proteins was inhibited. Had-2 cells had to be grown at higher cell densities in order to be NDV-resistant, and it was revealed that they did not exhibit NDV-resistance when grown at lower cell densities. A conditioned medium prepared from a culture of Had-2 cells grown at high cell density was able to make a low-density culture NDV-resistant. The activity of the conditioned medium to induce NDV-resistance was completely neutralized by addition of both anti interferon (IFN)-alpha and anti IFN-beta antibodies, indicating that Had-2 cells were constitutively releasing IFNs, though their levels were rather low. Had-2 cells were also characterized by an increased sensitivity to IFNs as compared with the parental FM3A cells, since the conditioned medium containing IFNs did not render FM3A cells resistant to NDV.

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“…S-Adenosyl[methyl-3H]methionine (specific activity [10][11][12][13][14][15] Ci/ mmol; 1 Ci = 3.7 x 1010 becquerels) was purchased from New England Nuclear. Nucleosides and mono-and triphosphates were from Sigma.…”

Section: Methodsmentioning

confidence: 99%

“…The inhibition apparently involves the activation of an RNase that degrades mRNA (9)(10)(11)(12)(13). The enzymatic activity, 2,5-oligo(adenylate) synthetase, which synthesizes pppApApA from ATP in the presence of double-stranded RNA has also been found in extracts of interferon-treated chicken embryo, 3T6, and HeLa cells (11,14,15). It is also present in rabbit reticulocyte lysates (16) and, in low amounts, in a variety ofother cells and tissues that had not been pretreated with interferon (17).…”

mentioning

confidence: 97%

Inhibition of vaccinia mRNA methylation by 2',5'-linked oligo(adenylic acid) triphosphate.

Sharma¹,

Goswami²

1981

Proc. Natl. Acad. Sci. U.S.A.

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Extracts of interferon-treated cells synthesize unique 2',5'-linked oligo(adenylic acid) 5'-phosphates in the presence ofATP and double-stranded RNA. 2',5'-linked oligo(adenylic acid) 5'-triphosphate inhibits protein synthesis at nanomolar concentrations by activating RNase. We have observed that oligo(adenylic acid) 5'-monophosphate and 5'-triphosphate are potent inhibitors of vaccinia mRNA methylation in vitro. Both the methylation of the 5'-terminal guanine at the 7 position and the 2'-O-ribose methylation of the penultimate nucleoside are inhibited. Such inhibition of mRNA methylation is not due to degradation of the mRNA.

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Interferon-associated, dsRNA-dependent enzyme activities in a mutant 3T6 cell engaged in the semiconstitutive synthesis of interferon

Cited by 25 publications

References 15 publications

Activation of Double-stranded RNA-activated Protein Kinase (PKR) by Interferon-stimulated Gene 15 (ISG15) Modification Down-regulates Protein Translation

Activation of Double-stranded RNA-activated Protein Kinase (PKR) by Interferon-stimulated Gene 15 (ISG15) Modification Down-regulates Protein Translation

Isolation and characterization of a novel mutant mouse cell line resistant to Newcastle disease virus: constitutive interferon production and enhanced interferon sensitivity

Inhibition of vaccinia mRNA methylation by 2',5'-linked oligo(adenylic acid) triphosphate.

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