Source:http://linkedlifedata.com/resource/pubmed/id/20847938
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:dateCreated |
2010-9-17
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| pubmed:abstractText |
The ATR-Chk1 checkpoint pathway is activated by UV-induced DNA lesions and replication stress. Little was known about the spatio and temporal behaviour of the proteins involved, and we, therefore, examined the behaviour of the ATRIP-ATR and Rad9-Rad1-Hus1 putative DNA damage sensor complexes and the downstream effector kinase Chk1. We developed assays for the generation and validation of stable cell lines expressing GFP-fusion proteins. Photobleaching experiments in living cells expressing these fusions indicated that after UV-induced DNA damage, ATRIP associates more transiently with damaged chromatin than members of the Rad9-Rad1-Hus1 complex. Interestingly, ATRIP directly associated with locally induced UV damage, whereas Rad9 bound in a cooperative manner, which can be explained by the Rad17-dependent loading of Rad9 onto damaged chromatin. Although Chk1 dissociates from the chromatin upon UV damage, no change in the mobility of GFP-Chk1 was observed, supporting the notion that Chk1 is a highly dynamic protein.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:status |
PubMed-not-MEDLINE
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| pubmed:issn |
2090-021X
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
2010
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:year |
2010
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| pubmed:articleTitle |
Differential Dynamics of ATR-Mediated Checkpoint Regulators.
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| pubmed:affiliation |
Department of Cell Biology and Genetics, Cancer Genome Center, Erasmus MC, Dr. Molewaterplein 50, 3015 GE Rotterdam, The Netherlands.
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| pubmed:publicationType |
Journal Article
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