Linked Life Data

18947885

Source:http://linkedlifedata.com/resource/pubmed/id/18947885

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2008-11-25
pubmed:abstractText
Inflammatory cytokines, produced mainly by activated microglia in the brain, can enhance neuronal degeneration and the amyloid-beta-plaque production involved in Alzheimer's disease (AD). We previously demonstrated that the expression of the pro-inflammatory cytokine interleukin-18 (IL-18) colocalizes with plaques and hyperphoshorylated tau containing neurons in AD patients. Here we exposed neuron-like, differentiated SH-SY5Y neuroblastomas to IL-18 and observed that the protein levels of p35, Cdk5, GSK-3beta, and Ser15-phosphorylated p53 increased during 6 h-24 h. Tau phosphorylation and expression of cyclin G1, involved in neuronal regeneration, increased at 72 h. In vivo, over-expression of IL-18 may induce hyperphosphorylation of tau and induce cell cycle activators.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0165-5728
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
205
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
86-93
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Interleukin-18 increases expression of kinases involved in tau phosphorylation in SH-SY5Y neuroblastoma cells.
pubmed:affiliation
University of Kuopio, Institute of Clinical Medicine/Neurology, Canthia, P.O.B. 1627, FIN-70211 Kuopio, Finland. Johanna.Ojala@uku.fi
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't