Nucleic Acids Research Advance Access originally published online on February 8, 2007
Nucleic Acids Research 2007 35(5):1569-1577; doi:10.1093/nar/gkl1159
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Nucleic Acids Research, 2007, Vol. 35, No. 5 1569-1577
© 2007 The Author(s).
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Molecular Biology |
Human base excision repair complex is physically associated to DNA replication and cell cycle regulatory proteins
1Department of Environment and Primary Prevention, Section of Molecular Epidemiology, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy and 2DNA Enzymology and Molecular Virology, Istituto di Genetica Molecolare, IGM-CNR, National Research Council, Via Abbiategrasso 207, 27100 Pavia, Italy
*To whom correspondence should be addressed. Tel: (+39) 0382546354; Fax: (+39) 0382422286; Email: maga{at}igm.cnr.it
Received August 31, 2006. Accepted December 19, 2006.
It has been hypothesized that a replication associated repair pathway operates on base damage and single strand breaks (SSB) at replication forks. In this study, we present the isolation from the nuclei of human cycling cells of a multiprotein complex containing most of the essential components of base excision repair (BER)/SSBR, including APE1, UNG2, XRCC1 and POLß, DNA PK, replicative POL
, 
and 
, DNA ligase 1 and cell cycle regulatory protein cyclin A. Co-immunoprecipitation revealed that in this complex DNA repair proteins are physically associated to cyclin A and to DNA replication proteins including MCM7. This complex is endowed with DNA polymerase and protein kinase activity and is able to perform BER of uracil and AP sites. This finding suggests that a preassembled DNA repair machinery is constitutively active in cycling cells and is ready to be recruited at base damage and breaks occurring at replication forks.
The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors.
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