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- Publisher Website: 10.1073/pnas.92.19.8841
- Scopus: eid_2-s2.0-0029051672
- PMID: 7568028
- WOS: WOS:A1995RU75900063
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Article: Involvement of the double-stranded-RNA-dependent kinase PKR in interferon expression and interferon-mediated antiviral activity
Title | Involvement of the double-stranded-RNA-dependent kinase PKR in interferon expression and interferon-mediated antiviral activity |
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Authors | |
Issue Date | 1995 |
Publisher | National Academy of Sciences. The Journal's web site is located at http://www.pnas.org |
Citation | Proceedings Of The National Academy Of Sciences Of The United States Of America, 1995, v. 92 n. 19, p. 8841-8845 How to Cite? |
Abstract | The signaling mechanisms responsible for the induced expression of interferon (IFN) genes by vital infection or double-stranded RNA (dsRNA) are not well understood. Here we investigate the role of the interferon-induced dsRNA-dependent protein kinase PKR in the regulation of IFN induction. Biological activities attributed to PKR include regulating protein synthesis, mediating IFN actions, and functioning as a possible tumor suppressor. Since binding of dsRNA is required for its activation, PKR has been considered as a candidate signal transducer for regulating IFN expression. To examine this role of PKR, loss-of-function phenotypes in stable transformants of promonocytic U-937 cells were achieved by two different strategies, overexpression of an antisense PKR transcript or a dominant negative PKR mutant gene. Both types of PKR-deficient cells were more permissive for viral replication than the control U-937 cells. As the result of PKR loss, they also showed impaired induction of IFN-α and IFN-β genes in response to several inducers-specifically, encephalomyocarditis virus, lipopolysaccharide, and phorbol 12-myristate 13-acetate. Interestingly, while IFN-α induction by dsRNA was impaired in PKR-deficient cells, IFN-β induction remained intact. Loss of PKR function also resulted in decreased antiviral activity as elicited by IFN-α and, to a greater extent, by IFN- γ. These results implicate PKR in the regulation of several antiviral activities. |
Persistent Identifier | http://hdl.handle.net/10722/170280 |
ISSN | 2023 Impact Factor: 9.4 2023 SCImago Journal Rankings: 3.737 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Der, SD | en_US |
dc.contributor.author | Lau, AS | en_US |
dc.date.accessioned | 2012-10-30T06:07:12Z | - |
dc.date.available | 2012-10-30T06:07:12Z | - |
dc.date.issued | 1995 | en_US |
dc.identifier.citation | Proceedings Of The National Academy Of Sciences Of The United States Of America, 1995, v. 92 n. 19, p. 8841-8845 | en_US |
dc.identifier.issn | 0027-8424 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/170280 | - |
dc.description.abstract | The signaling mechanisms responsible for the induced expression of interferon (IFN) genes by vital infection or double-stranded RNA (dsRNA) are not well understood. Here we investigate the role of the interferon-induced dsRNA-dependent protein kinase PKR in the regulation of IFN induction. Biological activities attributed to PKR include regulating protein synthesis, mediating IFN actions, and functioning as a possible tumor suppressor. Since binding of dsRNA is required for its activation, PKR has been considered as a candidate signal transducer for regulating IFN expression. To examine this role of PKR, loss-of-function phenotypes in stable transformants of promonocytic U-937 cells were achieved by two different strategies, overexpression of an antisense PKR transcript or a dominant negative PKR mutant gene. Both types of PKR-deficient cells were more permissive for viral replication than the control U-937 cells. As the result of PKR loss, they also showed impaired induction of IFN-α and IFN-β genes in response to several inducers-specifically, encephalomyocarditis virus, lipopolysaccharide, and phorbol 12-myristate 13-acetate. Interestingly, while IFN-α induction by dsRNA was impaired in PKR-deficient cells, IFN-β induction remained intact. Loss of PKR function also resulted in decreased antiviral activity as elicited by IFN-α and, to a greater extent, by IFN- γ. These results implicate PKR in the regulation of several antiviral activities. | en_US |
dc.language | eng | en_US |
dc.publisher | National Academy of Sciences. The Journal's web site is located at http://www.pnas.org | en_US |
dc.relation.ispartof | Proceedings of the National Academy of Sciences of the United States of America | en_US |
dc.subject.mesh | Base Sequence | en_US |
dc.subject.mesh | Dna, Antisense | en_US |
dc.subject.mesh | Encephalomyocarditis Virus - Drug Effects - Growth & Development | en_US |
dc.subject.mesh | Gene Expression Regulation | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Interferon-Alpha - Biosynthesis - Pharmacology | en_US |
dc.subject.mesh | Interferon-Beta - Biosynthesis - Pharmacology | en_US |
dc.subject.mesh | Interferons - Biosynthesis - Pharmacology | en_US |
dc.subject.mesh | Molecular Sequence Data | en_US |
dc.subject.mesh | Monocytes - Enzymology - Metabolism | en_US |
dc.subject.mesh | Mutation | en_US |
dc.subject.mesh | Protein-Serine-Threonine Kinases - Biosynthesis - Deficiency - Genetics | en_US |
dc.subject.mesh | Suppression, Genetic | en_US |
dc.subject.mesh | Virus Replication - Drug Effects | en_US |
dc.subject.mesh | Eif-2 Kinase | en_US |
dc.title | Involvement of the double-stranded-RNA-dependent kinase PKR in interferon expression and interferon-mediated antiviral activity | en_US |
dc.type | Article | en_US |
dc.identifier.email | Lau, AS:asylau@hku.hk | en_US |
dc.identifier.authority | Lau, AS=rp00474 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1073/pnas.92.19.8841 | en_US |
dc.identifier.pmid | 7568028 | - |
dc.identifier.scopus | eid_2-s2.0-0029051672 | en_US |
dc.identifier.volume | 92 | en_US |
dc.identifier.issue | 19 | en_US |
dc.identifier.spage | 8841 | en_US |
dc.identifier.epage | 8845 | en_US |
dc.identifier.isi | WOS:A1995RU75900063 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Der, SD=7003963925 | en_US |
dc.identifier.scopusauthorid | Lau, AS=7202626202 | en_US |
dc.identifier.issnl | 0027-8424 | - |