|
rdf:type |
|
|
lifeskim:mentions |
umls-concept:C0007600,
umls-concept:C0017262,
umls-concept:C0023175,
umls-concept:C0026882,
umls-concept:C0029463,
umls-concept:C0043393,
umls-concept:C0079419,
umls-concept:C0086418,
umls-concept:C0162638,
umls-concept:C0162735,
umls-concept:C0185117,
umls-concept:C0205245,
umls-concept:C0249197,
umls-concept:C0442726,
umls-concept:C1510438,
umls-concept:C1511790,
umls-concept:C1522790,
umls-concept:C1705522,
umls-concept:C2911684,
umls-concept:C2924612
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|
pubmed:issue |
4
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|
pubmed:dateCreated |
1999-11-30
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|
pubmed:abstractText |
The 123A point mutation of p53 showed increased radiosensitivity, whereas other mutations (143A, 175H, and 273H) were not affected. To determine the reason for increased radiosensitivity of the 123A mutation, the response of the transformant of 123A mutation to ionizing radiation (IR) was examined and compared to those of transformants with the wild type p53 or other point mutations (143A, 175H, and 273H).
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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 |
1
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pubmed:volume |
45
|
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
975-80
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10571205-Apoptosis,
pubmed-meshheading:10571205-Cyclin-Dependent Kinase Inhibitor p21,
pubmed-meshheading:10571205-Cyclins,
pubmed-meshheading:10571205-Gene Expression Regulation,
pubmed-meshheading:10571205-Genes, p53,
pubmed-meshheading:10571205-Humans,
pubmed-meshheading:10571205-Neoplasm Proteins,
pubmed-meshheading:10571205-Osteosarcoma,
pubmed-meshheading:10571205-Point Mutation,
pubmed-meshheading:10571205-Radiation Tolerance,
pubmed-meshheading:10571205-Radiobiology,
pubmed-meshheading:10571205-Tumor Cells, Cultured,
pubmed-meshheading:10571205-Tumor Suppressor Protein p53
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pubmed:year |
1999
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pubmed:articleTitle |
A point mutation of human p53, which was not detected as a mutation by a yeast functional assay, led to apoptosis but not p21Waf1/Cip1/Sdi1 expression in response to ionizing radiation in a human osteosarcoma cell line, Saos-2.
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pubmed:affiliation |
Department of Radiation Biophysics, Atomic Bomb Disease Institute, Nagasaki University School of Medicine, Japan. okaichi@net.nagasaki-u.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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