| pubmed-article:9765401 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9765401 | lifeskim:mentions | umls-concept:C0206558 | lld:lifeskim |
| pubmed-article:9765401 | lifeskim:mentions | umls-concept:C0031715 | lld:lifeskim |
| pubmed-article:9765401 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:9765401 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
| pubmed-article:9765401 | lifeskim:mentions | umls-concept:C0017963 | lld:lifeskim |
| pubmed-article:9765401 | lifeskim:mentions | umls-concept:C0083982 | lld:lifeskim |
| pubmed-article:9765401 | lifeskim:mentions | umls-concept:C1136317 | lld:lifeskim |
| pubmed-article:9765401 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:9765401 | lifeskim:mentions | umls-concept:C1321758 | lld:lifeskim |
| pubmed-article:9765401 | lifeskim:mentions | umls-concept:C0872251 | lld:lifeskim |
| pubmed-article:9765401 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:9765401 | pubmed:dateCreated | 1998-11-5 | lld:pubmed |
| pubmed-article:9765401 | pubmed:abstractText | In herpes simplex virus-infected cells, viral gamma134.5 protein blocks the shutoff of protein synthesis by activated protein kinase R (PKR) by directing the protein phosphatase 1alpha to dephosphorylate the alpha subunit of eukaryotic translation initiation factor 2 (eIF-2alpha). The amino acid sequence of the gamma134.5 protein which interacts with the phosphatase has high homology to a domain of the eukaryotic protein GADD34. A class of compensatory mutants characterized by a deletion which results in the juxtaposition of the alpha47 promoter next to US11, a gamma2 (late) gene in wild-type virus-infected cells, has been described. In cells infected with these mutants, protein synthesis continues even in the absence of the gamma134.5 gene. In these cells, PKR is activated but eIF-2alpha is not phosphorylated, and the phosphatase is not redirected to dephosphorylate eIF-2alpha. We report the following: (i) in cells infected with these mutants, US11 protein was made early in infection; (ii) US11 protein bound PKR and was phosphorylated; (iii) in in vitro assays, US11 blocked the phosphorylation of eIF-2alpha by PKR activated by poly(I-C); and (iv) US11 was more effective if present in the reaction mixture during the activation of PKR than if added after PKR had been activated by poly(I-C). We conclude the following: (i) in cells infected with the compensatory mutants, US11 made early in infection binds to PKR and precludes the phosphorylation of eIF-2alpha, whereas US11 driven by its natural promoter and expressed late in infection is ineffective; and (ii) activation of PKR by double-stranded RNA is a common impediment countered by most viruses by different mechanisms. The gamma134.5 gene is not highly conserved among herpesviruses. A likely scenario is that acquisition by a progenitor of herpes simplex virus of a portion of the cellular GADD34 gene resulted in a more potent and reliable means of curbing the effects of activated PKR. US11 was retained as a gamma2 gene because, like many viral proteins, it has multiple functions. | lld:pubmed |
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| pubmed-article:9765401 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9765401 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9765401 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9765401 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:9765401 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9765401 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:9765401 | pubmed:issn | 0022-538X | lld:pubmed |
| pubmed-article:9765401 | pubmed:author | pubmed-author:GrossMM | lld:pubmed |
| pubmed-article:9765401 | pubmed:author | pubmed-author:RoizmanBB | lld:pubmed |
| pubmed-article:9765401 | pubmed:author | pubmed-author:CassadyK AKA | lld:pubmed |
| pubmed-article:9765401 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9765401 | pubmed:volume | 72 | lld:pubmed |
| pubmed-article:9765401 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9765401 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9765401 | pubmed:pagination | 8620-6 | lld:pubmed |
| pubmed-article:9765401 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:9765401 | pubmed:meshHeading | pubmed-meshheading:9765401-... | lld:pubmed |
| pubmed-article:9765401 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9765401 | pubmed:articleTitle | The herpes simplex virus US11 protein effectively compensates for the gamma1(34.5) gene if present before activation of protein kinase R by precluding its phosphorylation and that of the alpha subunit of eukaryotic translation initiation factor 2. | lld:pubmed |
| pubmed-article:9765401 | pubmed:affiliation | The Marjorie B. Kovler Viral Oncology Laboratories, The University of Chicago, Chicago, Illinois 60637, USA. | lld:pubmed |
| pubmed-article:9765401 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9765401 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
