@article{oai:repo.qst.go.jp:00047889,
 author = {Yoneshima, Yasuto and Abolhassani, Nona and Iyama, Teruaki and Sakumi, Kunihiko and Shiomi, Naoko and Mori, Masahiko and Shiomi, Tadahiro and Noda, Tetsuo and Tsuchimoto, Daisuke and Nakabeppu, Yusaku and 塩見 尚子 and 森 雅彦 and 塩見 忠博},
 journal = {Scientific reports},
 month = {Apr},
 note = {Deoxyinosine (dI) occurs in DNA either by oxidative deamination of a previously incorporated deoxyadenosine residue or by misincorporation of deoxyinosine triphosphate (dITP) from the nucleotide pool during replication. To exclude dITP from the pool, mammals possess specific hydrolysing enzymes, such as inosine triphosphatase (ITPA). Previous studies have shown that deficiency in ITPA results in cell growth suppression and DNA instability. To explore the mechanisms of these phenotypes, we analysed ITPA-deficient human and mouse cells. We found that both growth suppression and accumulation of single-strand breaks in nuclear DNA of ITPA-deficient cells depended on MLH1/PMS2. The cell growth suppression of ITPA-deficient cells also depended on p53, but not on MPG, ENDOV or MSH2. ITPA deficiency significantly increased the levels of p53 protein and p21 mRNA/protein, a well-known target of p53, in an MLH1-dependent manner. Furthermore, MLH1 may also contribute to cell growth arrest by increasing the basal level of p53 activity.},
 pages = {32849-1--32849-16},
 title = {Deoxyinosine triphosphate induces MLH1/PMS2- and p53-dependent cell growth arrest and DNA instability in mammalian cells.},
 volume = {6},
 year = {2017}
}