Linked Life Data

9368285

Source:http://linkedlifedata.com/resource/pubmed/id/9368285

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1998-1-15
pubmed:abstractText
The most common mechanism by which radiation kills cells is the induction of DNA double-strand breaks that results in the loss of cell proliferation. Even though apoptosis is increasingly identified in experimental systems in vitro and in vivo, it is still generally regarded as a rare mode of radiation-induced cell kill with minor relevance for the clinical effects of radiation. This review will focus on pro- and antiapoptotic signaling that affects the apoptotic outcome in irradiated mammalian cells. In particular, we will concentrate on the sphingomyelin/ceramide signal transduction pathway which is involved in initiation of stress-induced apoptosis in a variety of normal and neoplastic cells. We will also discuss the crosstalk between the sphingomyelin/ceramide pathway and the protein kinase C pathway which constitutes an antiapoptotic pathway, and the potential for pharmacological modulation to increase the fraction of apoptotic cells undergoing apoptosis after radiation exposure.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1066-5099
pubmed:author
pubmed:issnType
Print
pubmed:volume
15 Suppl 2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
43-7
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Differential inhibition of radiation-induced apoptosis.
pubmed:affiliation
Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review