Linked Life Data

18042254

Source:http://linkedlifedata.com/resource/pubmed/id/18042254

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-2-8
pubmed:abstractText
Autonomous parvoviruses are strongly dependent on the phosphorylation of the major non-structural protein NS1 by members of the protein kinase C (PKC) family. Besides being accompanied with changes in the overall phosphorylation pattern of NS1 and acquiring new modifications at consensus PKC sites, ongoing minute virus of mice (MVM) infections lead to the appearance of new phosphorylated cellular protein species. This prompted us to investigate whether MVM actively interferes with phosphoinositol-dependent kinase (PDK)/PKC signalling. The activity, subcellular localization and phosphorylation status of the protein kinases PDK1, PKCeta and PKClambda were measured in A9 cells in the presence or absence of MVM infection. Parvovirus infection was found to result in activation of both PDK1 and PKCeta, as evidenced by changes in their subcellular distribution and overall (auto)phosphorylation. We show evidence that activation of PKCeta by PDK1 is driven by atypical PKClambda. By modifying the hydrophobic motif of PKCeta, PKClambda appeared to control docking and consecutive phosphorylation of PKCeta's activation-loop by PDK1, a process that was inhibited in vivo in the presence of a dominant-negative PKClambda mutant.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1462-5822
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
755-69
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Parvovirus interference with intracellular signalling: mechanism of PKCeta activation in MVM-infected A9 fibroblasts.
pubmed:affiliation
Program 'Infection and Cancer', Abteilung F010 and Institut National de la Santé et de la Recherche Médicale U701, Deutsches Krebsforschungszentrum, Heidelberg, Germany.
pubmed:publicationType
Journal Article