Linked Life Data

17377498

Source:http://linkedlifedata.com/resource/pubmed/id/17377498

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2007-4-4
pubmed:abstractText
The induction of cell death by radiation has largely been attributed to pro-apoptotic mechanisms. Autophagy, an alternative form of programmed cell death, has recently been shown to contribute significantly to anti-neoplastic effects of radiation therapy. In light of this, ER stress has been shown to trigger both apoptosis and autophagy, and act as an important mediator linking the two programmed cell death pathways. Recent data reveal that ER stress leads to activation of autophagosome formation with LC3 conversion via either PERK-eIF2a pathway or IRE1-JNK pathway. In this focused review, we summarize the main molecular mediators that control cellular "switches" between apoptosis and autophagy pathways by utilizing radiation therapy as a model.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1551-4005
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
793-8
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Switch between apoptosis and autophagy: radiation-induced endoplasmic reticulum stress?
pubmed:affiliation
Department of Radiation Oncology, Vanderbilt Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee 37232, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Review, Research Support, Non-U.S. Gov't