Eri Inoue
Tohoku University
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Publication
Featured researches published by Eri Inoue.
Molecular Cell | 2012
Tatsuhisa Tsuboi; Kazushige Kuroha; Kazuhei Kudo; Shiho Makino; Eri Inoue; Isao Kashima; Toshifumi Inada
Translation arrest leads to an endonucleolytic cleavage of mRNA that is termed no-go decay (NGD). It has been reported that the Dom34:Hbs1 complex stimulates this endonucleolytic cleavage of mRNA induced by translation arrest in vivo and dissociates subunits of a stalled ribosome in vitro. Here we report that Dom34:Hbs1 dissociates the subunits of a ribosome that is stalled at the 3 end of mRNA in vivo, and has a crucial role in both NGD and nonstop decay. Dom34:Hbs1-mediated dissociation of a ribosome that is stalled at the 3 end of mRNA is required for degradation of a 5-NGD intermediate. Dom34:Hbs1 facilitates the decay of nonstop mRNAs from the 3 end by exosomes and is required for the complete degradation of nonstop mRNA decay intermediates. We propose that Dom34:Hbs1 stimulates degradation of the 5-NGD intermediate and of nonstop mRNA by dissociating the ribosome that is stalled at the 3 end of the mRNA.
Journal of Nucleic Acids | 2010
Eri Inoue; Keizo Tano; Hanako Yoshii; Jun Nakamura; Shusuke Tada; Masami Watanabe; Masayuki Seki; Takemi Enomoto
Reactive oxygen species (ROSs) are produced during normal cellular metabolism, particularly by respiration in mitochondria, and these ROSs are considered to cause oxidative damage to macromolecules, including DNA. In our previous paper, we found no indication that depletion of mitochondrial superoxide dismutase, SOD2, resulted in an increase in DNA damage. In this paper, we examined SOD1, which is distributed in the cytoplasm, nucleus, and mitochondrial intermembrane space. We generated conditional SOD1 knockout cells from chicken DT40 cells and analyzed their phenotypes. The results revealed that SOD1 was essential for viability and that depletion of SOD1, especially nuclear SOD1, increased sister chromatid exchange (SCE) frequency, suggesting that superoxide is generated in or near the nucleus and that nuclear SOD1 functions as a guardian of the genome. Furthermore, we found that ascorbic acid could offset the defects caused by SOD1 depletion, including cell lethality and increases in SCE frequency and apurinic/apyrimidinic sites.
Journal of Cell Biology | 2007
Makoto Otsuki; Masayuki Seki; Eri Inoue; Akari Yoshimura; Genta Kato; Saki Yamanouchi; Yoh Ichi Kawabe; Shusuke Tada; Akira Shinohara; Jun Ichiro Komura; Tetsuya Ono; Shunichi Takeda; Yutaka Ishii; Takemi Enomoto
Blooms syndrome (BS), which is caused by mutations in the BLM gene, is characterized by a predisposition to a wide variety of cancers. BS cells exhibit elevated frequencies of sister chromatid exchanges (SCEs), interchanges between homologous chromosomes (mitotic chiasmata), and sensitivity to several DNA-damaging agents. To address the mechanism that confers these phenotypes in BS cells, we characterize a series of double and triple mutants with mutations in BLM and in other genes involved in repair pathways. We found that XRCC3 activity generates substrates that cause the elevated SCE in blm cells and that BLM with DNA topoisomerase IIIα suppresses the formation of SCE. In addition, XRCC3 activity also generates the ultraviolet (UV)- and methyl methanesulfonate (MMS)–induced mitotic chiasmata. Moreover, disruption of XRCC3 suppresses MMS and UV sensitivity and the MMS- and UV-induced chromosomal aberrations of blm cells, indicating that BLM acts downstream of XRCC3.
Free Radical Research | 2013
Yuki Tamari; Hisakatsu Nawata; Eri Inoue; Akari Yoshimura; Hanako Yoshii; Genro Kashino; Masayuki Seki; Takemi Enomoto; Masami Watanabe; Keizo Tano
Abstract Superoxide dismutases (SODs) are antioxidant proteins that convert superoxide to hydrogen peroxide. In vertebrate cells, SOD1 is mainly present in the cytoplasm, with small levels also found in the nucleus and mitochondrial intermembrane space, and SOD2 is present in the mitochondrial matrix. Previously, the authors conditionally disrupted the SOD1 or SOD2 gene in DT40 cells and found that depletion of SOD1 caused lethality, while depletion of SOD2 led to growth retardation. The observations from previous work showed that the lethality observed in SOD1-depleted cells was completely rescued by ascorbic acid. Ascorbic acid is a water-soluble antioxidant present in biological fluids; however, the exact target for its antioxidant effects is not known. In this study, the authors demonstrated that ascorbic acid offset growth defects observed in SOD2-depleted cells and also lowered mitochondrial superoxide to physiological levels in both SOD1- or SOD2-depleted cells. Moreover, depletion of SOD1 or SOD2 resulted in the accumulation of intracellular oxidative stress, and this increased oxidative stress was reduced by ascorbic acid. Taken together, this study suggests that ascorbic acid can be applied as a nontoxic antioxidant that mimics the functions of cytoplasmic and mitochondrial SODs.
Biochemical and Biophysical Research Communications | 2009
Shunya Takada; Eri Inoue; Keizo Tano; Hanako Yoshii; Takuya Abe; Akari Yoshimura; Motomu Akita; Shusuke Tada; Masami Watanabe; Masayuki Seki; Takemi Enomoto
Manganese-dependent superoxide dismutase (SOD2) serves as the primary defense against mitochondrial superoxide, and decreased SOD2 activity results in a range of pathologies. To investigate the events occurring soon after depletion of SOD2, we generated SOD2 gene knockout chicken DT40 cells complemented with a human SOD2 (hSOD2) cDNA, whose expression can be switched off by doxycycline (Dox). When SOD2 was depleted by the addition of Dox, the cells grew slightly slower and formed fewer colonies than cells expressing hSOD2. In addition, these cells showed a high sensitivity to paraquat, which produces superoxide, and died through apoptosis. In contrast to results obtained with mouse and DrosophilaSod2 mutants, we found no indication of an increase in DNA lesions due to depletion of SOD2.
Biochemical and Biophysical Research Communications | 2006
Parimal Karmakar; Masayuki Seki; Makoto Kanamori; Kazunari Hashiguchi; Makoto Ohtsuki; Eriko Murata; Eri Inoue; Shusuke Tada; Li Lan; Akira Yasui; Takemi Enomoto
Biochemical and Biophysical Research Communications | 2007
Makoto Otsuki; Masayuki Seki; Yoh-ichi Kawabe; Eri Inoue; Yu Peng Dong; Takuya Abe; Genta Kato; Akari Yoshimura; Shusuke Tada; Takemi Enomoto
Genes & Genetic Systems | 2008
Tomoko Hayashi; Masayuki Seki; Eri Inoue; Akari Yoshimura; Yumiko Kusa; Shusuke Tada; Takemi Enomoto
Biochimica et Biophysica Acta | 2008
Makoto Otsuki; Masayuki Seki; Eri Inoue; Takuya Abe; Yoshiyasu Narita; Akari Yoshimura; Shusuke Tada; Yutaka Ishii; Takemi Enomoto
Biological & Pharmaceutical Bulletin | 2007
Yu Peng Dong; Masayuki Seki; Akari Yoshimura; Eri Inoue; Shinya Furukawa; Shusuke Tada; Takemi Enomoto