Linked Life Data

18301379

Source:http://linkedlifedata.com/resource/pubmed/id/18301379

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-3-3
pubmed:abstractText
Death receptors, including the TNF receptor-1 (TNF-RI), have been shown to be able to initiate caspase-independent cell death. This form of "necrotic cell death" appears to be dependent on the generation of reactive oxygen species. Recent data have indicated that superoxide generation is dependent on the activation of NADPH oxidases, which form a complex with the adaptor molecules RIP1 and TRADD. The mechanism of superoxide generation further establishes RIP1 as the central molecule in ROS production and cell death initiated by TNFalpha and other death receptors. A role for the sustained JNK activation in necrotic cell death is also suggested. The sensitization of virus-infected cells to TNFalpha indicates that necrotic cell death may represent an alternative cell death pathway for clearance of infected cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1748-7838
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
343-9
pubmed:dateRevised
2010-9-20
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
TNFalpha and reactive oxygen species in necrotic cell death.
pubmed:affiliation
Cell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Intramural