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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
2007-10-30
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pubmed:abstractText |
The molecular basis of low-dose hyper-radiosensitivity (HRS) is only partially understood. The aim of this study was to define the roles of ataxia telangiectasia mutated (ATM) activity and the downstream ATM-dependent G(2)-phase cell cycle checkpoint in overcoming HRS and triggering radiation resistance.
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pubmed:grant |
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0360-3016
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
69
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1262-71
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pubmed:dateRevised |
2011-11-2
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pubmed:meshHeading |
pubmed-meshheading:17967316-Animals,
pubmed-meshheading:17967316-Cell Cycle Proteins,
pubmed-meshheading:17967316-Cell Line,
pubmed-meshheading:17967316-Cell Survival,
pubmed-meshheading:17967316-Cricetinae,
pubmed-meshheading:17967316-Cricetulus,
pubmed-meshheading:17967316-DNA-Binding Proteins,
pubmed-meshheading:17967316-G2 Phase,
pubmed-meshheading:17967316-Humans,
pubmed-meshheading:17967316-Protein-Serine-Threonine Kinases,
pubmed-meshheading:17967316-RNA, Small Interfering,
pubmed-meshheading:17967316-Radiation Dosage,
pubmed-meshheading:17967316-Radiation Tolerance,
pubmed-meshheading:17967316-Rats,
pubmed-meshheading:17967316-Tumor Suppressor Proteins
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pubmed:year |
2007
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pubmed:articleTitle |
Transition in survival from low-dose hyper-radiosensitivity to increased radioresistance is independent of activation of ATM Ser1981 activity.
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pubmed:affiliation |
Department of Radiation Oncology, Karmanos Cancer Institute, Wayne State University, Detroit, MI, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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