Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-7-4
pubmed:abstractText
The transcription factor E2F1 coordinates cell cycle progression and induces apoptosis in response to DNA damage stress. Aside from DNA damage, the role of E2F1 in the endoplasmic reticulum (ER) stress signaling pathways is unclear. We found that E2F1-/- murine embryonic fibroblasts (MEFs) are resistant to apoptosis triggered by the ER stress inducer thapsigargin. In addition, E2F1 deficiency results in enhanced phosphorylation of eukaryotic translation initiation factor 2a (eIF2a). These results therefore indicate that E2F1 deficiency increases phosphorylation of eIF2a in response to ER stress triggered by thapsigargin, and suggest that the reduction in ER stress-induced apoptosis in E2F1-deficient cells is related to the high level of eIF2a phosphorylation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1016-8478
pubmed:author
pubmed:issnType
Print
pubmed:day
30
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
356-9
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Role of E2F1 in endoplasmic reticulum stress signaling.
pubmed:affiliation
Functional Genomics Research Center, Division of Molecular Therapeutics, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-333, Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't