Linked Life Data

9006086

Source:http://linkedlifedata.com/resource/pubmed/id/9006086

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1997-2-13
pubmed:abstractText
The p53 tumor suppressor protein is rapidly induced following treatment of cells with agents which cause DNA double strand breaks (dsbs) leading to cell cycle arrest and/or apoptosis. Scid mutant mice are defective in repair of DNA dsbs which was recently shown to be due to lack of DNA-dependent protein kinase (DNAPK) activity. DNAPK is normally activated by DNA dsbs and phosphorylates the p53 protein. Here we tested the hypothesis that DNAPK transduces the signal from DNA dsbs to p53 induction. P53 protein was properly induced in intestinal crypt cells of irradiated scid mice and was functional as detected by the large increase in apoptotic cells. P53 induction was prolonged, consistent with DNA dsbs as the signal to induce p53. Spontaneous levels of apoptosis were elevated suggesting that scid mice are sensitive indicators of spontaneously generated DNA dsbs. Primary scid fibroblasts underwent normal G1 and G2 arrest in response to doxorubicin. DNAPK is not required for p53 induction, cell cycle arrest, or apoptosis after DNA damage.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0143-3334
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2537-42
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
p53 induction, cell cycle checkpoints, and apoptosis in DNAPK-deficient scid mice.
pubmed:affiliation
Fred Hutchinson Cancer Research Center, Seattle, WA 98104, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't