Linked Life Data

11724323

Source:http://linkedlifedata.com/resource/pubmed/id/11724323

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4A
pubmed:dateCreated
2001-11-28
pubmed:abstractText
c-jun-N-terminal kinases (JNKs) play an important role in defense against external stresses including ionizing radiation (IR). We have previously shown that sensitivity to IR is influenced by p53 status in human thyroid cells. In this study, we investigated the effect of p53 status on IR-induced JNK activation in human thyroid cells. Our results showed high basal JNK activity in the p53-null thyroid cancer cell line, FRO. In contrast, primary cultured thyroid cells (PT), which harbor wild-type p53, had low basal JNK activity. IR increased JNK activity in PT, however, no such increase was noted in FRO cells. Introduction of the wild-type p53 into FRO cells reduced JNK activity to a low basal level and rendered it responsive to IR. There was no difference in IR-induced ceramide production between PT and FRO cells. Our results provide clear evidence that p53 status influences, directly or indirectly, radiation-induced JNK activation in human thyroid cells, suggesting that a feedback or interaction pathway between p53 and JNK regulates radiation-induced cell fate.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0250-7005
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2569-75
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:articleTitle
Involvement of wild-type p53 in radiation-induced c-Jun N-terminal kinase activation in human thyroid cells.
pubmed:affiliation
Department of Nature Medicine, Atoic Bomb Disease Institute, Nagasaki University School of Medicine, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't