D788–D792 Nucleic Acids Research, 2011, Vol. 39, Database issue doi:10.1093/nar/gkq1087 Published online 4 November 2010 REPAIRtoire—a database of DNA repair pathways Kaja Milanowska1,2, Joanna Krwawicz3, Grzegorz Papaj1, Jan Kosin´ ski1,4, Katarzyna Poleszak 1 , Justyna Lesiak 1 , Ewelina Osin´ ska 1 , Kristian Rother1,2 and Janusz M. Bujnicki1,2,* 1Laboratory of Bioinformatics and Protein Engineering, International Institute of Molecular and Cell Biology, ul. Ks. Trojdena 4, 02-109 Warsaw, Poland, 2Laboratory of Bioinformatics, Institute of Molecular Biology and Biotechnology, Adam Mickiewicz University, ul. Umultowska 89, 61-614 Poznan, Poland, 3Department of Molecular Biology, Institute of Biochemistry and Biophysics Polish Academy of Sciences, 5A Pawinskiego, 02-106 Warsaw, Poland and 4Biocomputing group, Department of Biochemical Sciences, ‘‘Sapienza’’ University, P. le A. Moro, 5, 00185 Rome, Italy Received August 15, 2010; Revised October 14, 2010; Accepted October 15, 2010 ABSTRACT REPAIRtoire is the first comprehensive database resource for systems biology of DNA damage and repair. The database collects and organizes the fol- lowing types of information: (i) DNA damage linked to environmental mutagenic and cytotoxic agents, (ii) pathways comprising individual processes and enzymatic reactions involved in the removal of damage, (iii) proteins participating in DNA repair and (iv) diseases correlated with mutations in genes encoding DNA repair proteins. REPAIRtoire provides also links to publications and external databases. REPAIRtoire contains information about eight main DNA damage checkpoint, repair and tolerance pathways: DNA damage signaling, direct reversal repair, base excision repair, nucleo- tide excision repair, mismatch repair, homologous recombination repair, nonhomologous end-joining and translesion synthesis. The pathway/protein dataset is currently limited to three model organ- isms: Escherichia coli, Saccharomyces cerevisiae and Homo sapiens. The DNA repair and tolerance pathways are represented as graphs and in tabular form with descriptions of each repair step and corresponding proteins, and individual entries are cross-referenced to supporting literature and primary databases. REPAIRtoire can be queried by the name of pathway, protein, enzymatic complex, damage and disease. In addition, a tool for drawing custom DNA–protein complexes is available online. REPAIRtoire is freely available and can be accessed at http://repairtoire.genesilico.pl/. INTRODUCTION DNA repair processes are of crucial importance for the maintenance of the genetic information of all organisms. The stability of the genome is constantly endangered by environmental agents, endogenous metabolic processes, e.g. reactive species inside cells, and errors of cellular processes involving DNA. Modiﬁcations of DNA can lead to mutations, which alter the coding sequence of DNA and can lead to cancer in humans and other mammals. Other DNA lesions interfere with normal cellular transactions, such as DNA replication or tran- scription, and are deleterious to the cell (1,2). To counter- act DNA damage, organisms have evolved various damage prevention and repair systems (3–7). These systems ensure the stability of DNA and accurate trans- mission of genetic information by protecting the genome against a large number of different chemical and structural alterations. At the same time, random changes in DNA are viewed as a main source of genetic variability, and thus a driving force for evolution. In multicellular organisms changes in the DNA sequence and structure are respon- sible for e.g. differential production of antibodies by the immune system (8). Therefore, DNA repair mechanisms have to balance the noxious against the beneﬁcial effects of alterations in the genome sequence and chemical structure. It has been proposed that DNA damage from endogen- ous sources gives rise to 20 000 lesions per mammalian cell per day, most of the lesions being deaminations, *To whom correspondence should be addressed. Tel: +48 22 597 0750; Fax: +48 22 597 0715; Email: iamb@genesilico.pl The authors wish it to be known that, in their opinion, the ﬁrst three authors should be regarded as joint First Authors. The Author(s) 2010. Published by Oxford University Press. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/ by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.