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CHK2 kinase in the DNA damage response and beyond
Laura Zannini1, Domenico Delia1,*, and Giacomo Buscemi2,*
1Department of Experimental Oncology, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Amadeo 42, 20133 Milan, Italy
2Department of Biosciences, University of Milan, via Celoria 26, 20133 Milan, Italy *Correspondence to:Giacomo Buscemi, E-mail: giacomo.buscemi@unimi.it; Domenico Delia, E-mail: domenico.delia@istitutotumori.mi.it
J Mol Cell Biol, Volume 6, Issue 6, December 2014, Pages 442-457  https://doi.org/10.1093/jmcb/mju045
Keyword: DNA damage, checkpoints, apoptosis, genomic stability

The serine/threonine kinase CHK2 is a key component of the DNA damage response. In human cells, following genotoxic stress, CHK2 is activated and phosphorylates >20 proteins to induce the appropriate cellular response, which, depending on the extent of damage, the cell type, and other factors, could be cell cycle checkpoint activation, induction of apoptosis or senescence, DNA repair, or tolerance of the damage. Recently, CHK2 has also been found to have cellular functions independent of the presence of nuclear DNA lesions. In particular, CHK2 participates in several molecular processes involved in DNA structure modification and cell cycle progression. In this review, we discuss the activity of CHK2 in response to DNA damage and in the maintenance of the biological functions in unstressed cells. These activities are also considered in relation to a possible role of CHK2 in tumorigenesis and, as a consequence, as a target of cancer therapy.