rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2009-6-26
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pubmed:abstractText |
The tumor suppressor p53 is a critical component of the DNA damage response pathway that induces a set of genes responsible for cell cycle arrest, senescence, apoptosis, and DNA repair. The ataxia telangiectasia mutated protein kinase (ATM) responds to DNA-damage stimuli and signals p53 stabilization and activation, thereby facilitating transactivation of p53 inducible genes and maintainence of genome integrity. In this study, we identified a CXXC zinc finger domain containing protein termed CF5 as a critical component in the DNA damage signaling pathway. CF5 induces p53 transcriptional activity and apoptosis in cells expressing wild type p53 but not in p53-deficient cells. Knockdown of CF5 inhibits DNA damage-induced p53 activation as well as cell cycle arrest. Furthermore, CF5 physically interacts with ATM and is required for DNA damage-induced ATM phosphorylation but not its recruitment to chromatin. These findings suggest that CF5 plays a crucial role in ATM-p53 signaling in response to DNA damage.
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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 |
http://linkedlifedata.com/resource/pubmed/chemical/Antineoplastic Agents, Phytogenic,
http://linkedlifedata.com/resource/pubmed/chemical/CXXC5 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Cell Cycle Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Etoposide,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Protein p53,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/ataxia telangiectasia mutated...
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1006-9305
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:volume |
52
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
528-38
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pubmed:dateRevised |
2011-11-2
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pubmed:meshHeading |
pubmed-meshheading:19557330-Amino Acid Sequence,
pubmed-meshheading:19557330-Animals,
pubmed-meshheading:19557330-Antineoplastic Agents, Phytogenic,
pubmed-meshheading:19557330-Carrier Proteins,
pubmed-meshheading:19557330-Cell Cycle,
pubmed-meshheading:19557330-Cell Cycle Proteins,
pubmed-meshheading:19557330-DNA Damage,
pubmed-meshheading:19557330-DNA-Binding Proteins,
pubmed-meshheading:19557330-Etoposide,
pubmed-meshheading:19557330-Gene Expression Regulation,
pubmed-meshheading:19557330-HeLa Cells,
pubmed-meshheading:19557330-Humans,
pubmed-meshheading:19557330-Molecular Sequence Data,
pubmed-meshheading:19557330-Protein-Serine-Threonine Kinases,
pubmed-meshheading:19557330-RNA Interference,
pubmed-meshheading:19557330-Sequence Alignment,
pubmed-meshheading:19557330-Signal Transduction,
pubmed-meshheading:19557330-Tumor Suppressor Protein p53,
pubmed-meshheading:19557330-Tumor Suppressor Proteins,
pubmed-meshheading:19557330-Zinc Fingers
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pubmed:year |
2009
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pubmed:articleTitle |
The CXXC finger 5 protein is required for DNA damage-induced p53 activation.
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pubmed:affiliation |
College of Life Sciences, Peking University, Beijing 100871, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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