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rdf:type |
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lifeskim:mentions |
umls-concept:C0012860,
umls-concept:C0017337,
umls-concept:C0035647,
umls-concept:C0035820,
umls-concept:C0178539,
umls-concept:C0871261,
umls-concept:C1384666,
umls-concept:C1414006,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C2911692
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pubmed:issue |
8
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pubmed:dateCreated |
2006-8-31
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pubmed:abstractText |
The tumor suppressor p53 plays a crucial role in the cellular response to DNA damage by transcriptional activation of numerous downstream genes. Although a considerable number of p53 target genes have been reported, the precise mechanism of p53-regulated tumor suppression still remains to be elucidated. Here, we report a novel role of the DFNA5 gene in p53-mediated etoposide-induced cell death. The DFNA5 gene has been previously reported to be responsible for autosomal-dominant, nonsyndromic hearing impairment. The expression of the DFNA5 gene was strongly induced by exogenous and endogenous p53. The chromatin immunoprecipitation assay indicated that a potential p53-binding sequence is located in intron 1 of the DFNA5 gene. Furthermore, the reporter gene assay revealed that the sequence displays p53-dependent transcriptional activity. The ectopic expression of DFNA5 enhanced etoposide-induced cell death in the presence of p53; however, it was inhibited in the absence of p53. Finally, the expression of DFNA5 mRNA was remarkably induced by gamma-ray irradiation in the colon of p53(+/+) mice but not in that of p53(-/-) mice. These results suggest that DFNA5 plays a role in the p53-regulated cellular response to genotoxic stress probably by cooperating with p53.
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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:issn |
1434-5161
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pubmed:author |
pubmed-author:ArakawaHirofumiH,
pubmed-author:BabaHideoH,
pubmed-author:EgamiHiroshiH,
pubmed-author:FutamuraManabuM,
pubmed-author:IchikawaHitoshiH,
pubmed-author:KaminoHirokiH,
pubmed-author:KitamuraNoriakiN,
pubmed-author:KiyonoTohruT,
pubmed-author:MasudaYoshikoY,
pubmed-author:MiyamotoYujiY,
pubmed-author:NakamuraYasuyukiY,
pubmed-author:OhkiMisaoM,
pubmed-author:OhnishiShihoS,
pubmed-author:OhtaTsutomuT
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pubmed:issnType |
Print
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pubmed:volume |
51
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
652-64
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:16897187-Animals,
pubmed-meshheading:16897187-Apoptosis,
pubmed-meshheading:16897187-Base Sequence,
pubmed-meshheading:16897187-Binding Sites,
pubmed-meshheading:16897187-COS Cells,
pubmed-meshheading:16897187-Cercopithecus aethiops,
pubmed-meshheading:16897187-DNA Damage,
pubmed-meshheading:16897187-Etoposide,
pubmed-meshheading:16897187-Exons,
pubmed-meshheading:16897187-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:16897187-Genome, Human,
pubmed-meshheading:16897187-Hearing Loss,
pubmed-meshheading:16897187-Humans,
pubmed-meshheading:16897187-Mice,
pubmed-meshheading:16897187-Microarray Analysis,
pubmed-meshheading:16897187-Molecular Sequence Data,
pubmed-meshheading:16897187-Protein Transport,
pubmed-meshheading:16897187-RNA, Messenger,
pubmed-meshheading:16897187-Receptors, Estrogen,
pubmed-meshheading:16897187-Transcription, Genetic,
pubmed-meshheading:16897187-Tumor Cells, Cultured,
pubmed-meshheading:16897187-Tumor Suppressor Protein p53
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pubmed:year |
2006
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pubmed:articleTitle |
The potential role of DFNA5, a hearing impairment gene, in p53-mediated cellular response to DNA damage.
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pubmed:affiliation |
Cancer Medicine and Biophysics Division, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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