Linked Life Data

9268153

Source:http://linkedlifedata.com/resource/pubmed/id/9268153

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1997-9-9
pubmed:abstractText
The U(L)41 protein of herpes simplex virus 1 (HSV-1) is packaged into virions, and in newly infected cells the protein mediates indiscriminate degradation of mRNA, which causes a shutoff of protein synthesis. We report that in cells infected with mutant virus in which either alpha22/U(S)1.5 or U(L)13 had been deleted: (i) the shutoff of protein synthesis and the degradation of mRNA did not take place or were greatly reduced, and consistent with these observations (ii) cells infected with mutant viruses accumulated less U(L)41 mRNA and protein than cells infected with the parent virus; and (iii) purified virions from cells infected with deltaU(L)13 or delta alpha22/deltaU(S)1.5 viruses contained less U(L)41 protein than virions produced by the wild-type parent virus. We conclude that the failure of the U(L)13- mutant virus to shut off protein synthesis immediately after infection is due to the failure of posttranslational modification of infected cell protein 22 and/or the related U(S)1.5 protein by the U(L)13 protein kinase. The regulatory effect of U(L)13 on U(L)41 is indirect and not contingent on direct interaction of this protein with the U(L)41 protein.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0042-6822
pubmed:author
pubmed:issnType
Print
pubmed:day
4
pubmed:volume
234
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
226-34
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Infected cell protein 22 of herpes simplex virus 1 regulates the expression of virion host shutoff gene U(L)41.
pubmed:affiliation
The Marjorie B. Kovler Viral Oncology Laboratories, University of Chicago, Illinois 60637, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.