Linked Life Data

17986386

Source:http://linkedlifedata.com/resource/pubmed/id/17986386

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-11-26
pubmed:abstractText
Selenoprotein P (SeP) is the major selenoprotein in human plasma, acting as an antioxidant and serving the transport of selenium from the liver to extrahepatic tissues. We here demonstrate that the human SeP promoter responds to overexpression of FoxO1a as well as of a constitutively active form of FoxO1a. Two FoxO-responsive elements were identified and characterized by generation of point mutation and deletion constructs. Similarly, SeP mRNA was upregulated in response to activation of FoxO1a in rat hepatoma cells stably transfected with a hydroxytamoxifen-regulatable form of FoxO1a. Insulin, stimulating the phosphorylation and inactivation of FoxO1a via phosphoinositide 3-kinase (PI3K) and Akt, suppressed SeP promoter activity and mRNA synthesis. This suppressive effect of insulin on SeP expression was attenuated by inhibitors of PI3K. In conclusion, the selenoprotein P promoter is a target of the Akt/FoxO signal transduction cascade and SeP expression is regulated at the level of transcription by the forkhead box protein FoxO1a in human and rat hepatoma cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1090-2104
pubmed:author
pubmed:issnType
Electronic
pubmed:day
11
pubmed:volume
365
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
316-21
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Stimulation of selenoprotein P promoter activity in hepatoma cells by FoxO1a transcription factor.
pubmed:affiliation
Institut für Biochemie und Molekularbiologie I, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't