Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
50
pubmed:dateCreated
2002-10-25
pubmed:abstractText
In response to replication block or DNA damage in S phase the DNA replication and DNA damage checkpoints are activated. The current model in human predicts, that a Rad17/Replication factor C (RF-C) complex might serve as a recruitment complex for the Rad9/Hus1/Rad1 complex to sites of replication block or DNA damage. In this study we have investigated the fate of the Rad17/RF-C complex after treatment of synchronized Hela cells with the replication inhibitor hydroxyurea. In hydroxyurea treated cells the RF-C p37 subunit became more resistant to extraction. Moreover, co-immunoprecipitation studies with extracts of hydroxyurea treated cells showed an interaction of RF-C p37 with Rad17 and of PCNA with Rad9 and RF-C p37. An enhanced colocalization of Rad17 and PCNA in late S phase after hydroxyurea treatment was observed. Our data suggested, that upon replication block a Rad17/RF-C complex is recruited to sites of DNA lesions in late S phase, binds the Rad9/Hus1/Rad1 complex and enables it to interact with PCNA. An interaction of Rad17/RF-C with PCNA appears to be mediated by the small RF-C p37 subunit, suggesting that PCNA might provide communication between replication checkpoint control and DNA replication and repair.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
31
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7710-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Colocalization of human Rad17 and PCNA in late S phase of the cell cycle upon replication block.
pubmed:affiliation
Institute of Veterinary Biochemistry and Molecular Biology, University Zürich-Irchel, Winterthurerstrasse 190, 8057 Zürich, Switzerland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't