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Suzuka, Japan

Suzuka University of Medical Science is a private university in Suzuka, Mie, Japan, established in 1991. The present name was adopted in 1998. Wikipedia.


Satomi Y.,Suzuka University of Medical Science
Anticancer Research | Year: 2012

Background/Aim: The antitumor effect of fucoxanthin, a marine carotenoid found in brown algae, was investigated on prostate cancer cells. Materials and Methods: LNCap prostate cancer cells were treated with fucoxanthin and the effects were evaluated in relation to cell proliferation, cell cycle, expression of growth arrest, DNA damage-inducible protein (GADD45) genes, and phosphorylation status of mitogen-activated protein kinases. Results: Fucoxanthin inhibited the growth of LNCap prostate cancer cells in a dose-dependent manner. Growth-inhibitory effects were accompanied by the induction of GADD45A expression and G 1 cell cycle arrest, but not apoptosis. Furthermore, fucoxanthin activated c-Jun N-terminal kinase (SAPK/JNK), while the inhibition of SAPK/JNK attenuated the induction of G 1 arrest and GADD45A expression by fucoxanthin. Conclusion: These results show that fucoxanthin induces G 1 cell cycle arrest in prostate cancer cells, and suggest that GADD45A and SAPK/JNK might be involved in these effects. Source


Maki K.,Nagoya University | Morita T.,Suzuka University of Medical Science | Otaka H.,Nagoya University | Aiba H.,Nagoya University
Molecular Microbiology | Year: 2010

Escherichia coli SgrS is an Hfq-binding small RNA that is induced under glucose-phosphate stress to cause translational repression and RNase E-dependent rapid degradation of ptsG mRNA encoding the major glucose transporter. A 31-nt-long stretch in the 3′ region of SgrS is partially complementary to the translation initiation region of ptsG mRNA. We showed previously that SgrS alone causes translational repression when pre-annealed with ptsG mRNA by a high-temperature treatment in vitro. Here, we studied translational repression of ptsG mRNA in vitro by synthetic RNA oligonucleotides (oligos) to define the SgrS region required for translational repression. We first demonstrate that a 31 nt RNA oligo corresponding to the base-pairing region is sufficient for translational inhibition of ptsG mRNA. Then, we show that RNA oligo can be shortened to 14 nt without losing its effect. Evidence shows that the 14 nt base-pairing region is sufficient to inhibit ptsG translation in the context of full-length SgrS in vivo. We conclude that SgrS 168-181 is a minimal base-pairing region for translational inhibition of ptsG mRNA. Interestingly, the 14 nt oligo efficiently inhibited ptsG translation without the high-temperature pre-treatment, suggesting that remodelling of structured SgrS is an important mechanism by which Hfq promotes the base pairing. © 2010 Blackwell Publishing Ltd. Source


Komeda S.,Suzuka University of Medical Science
Metallomics | Year: 2011

Platinum coordination compounds are among the most utilized anticancer agents, even though platinum has not been determined to be an essential trace element in any living organism. The success of platinum-based drugs has catalyzed research on other metal-containing agents that can be used to achieve therapeutic goals that cannot be achieved with organic compounds. The antitumor activities of recently reported platinum(ii) complexes indicate that further modification of platinum coordination compounds will lead to the development of anticancer agents with higher efficacies against chemotherapy-insensitive tumors. © 2011 The Royal Society of Chemistry. Source


Miyazaki T.,Nagasaki University | Nakayama H.,Suzuka University of Medical Science | Nagayoshi Y.,Nagasaki University | Kakeya H.,Nagasaki University | Kohno S.,Nagasaki University
PLoS Pathogens | Year: 2013

Proper protein folding in the endoplasmic reticulum (ER) is vital in all eukaryotes. When misfolded proteins accumulate in the ER lumen, the transmembrane kinase/endoribonuclease Ire1 initiates splicing of HAC1 mRNA to generate the bZIP transcription factor Hac1, which subsequently activates its target genes to increase the protein-folding capacity of the ER. This cellular machinery, called the unfolded protein response (UPR), is believed to be an evolutionarily conserved mechanism in eukaryotes. In this study, we comprehensively characterized mutant phenotypes of IRE1 and other related genes in the human fungal pathogen Candida glabrata. Unexpectedly, Ire1 was required for the ER stress response independently of Hac1 in this fungus. C. glabrata Ire1 did not cleave mRNAs encoding Hac1 and other bZIP transcription factors identified in the C. glabrata genome. Microarray analysis revealed that the transcriptional response to ER stress is not mediated by Ire1, but instead is dependent largely on calcineurin signaling and partially on the Slt2 MAPK pathway. The loss of Ire1 alone did not confer increased antifungal susceptibility in C. glabrata contrary to UPR-defective mutants in other fungi. Taken together, our results suggest that the canonical Ire1-Hac1 UPR is not conserved in C. glabrata. It is known in metazoans that active Ire1 nonspecifically cleaves and degrades a subset of ER-localized mRNAs to reduce the ER load. Intriguingly, this cellular response could occur in an Ire1 nuclease-dependent fashion in C. glabrata. We also uncovered the attenuated virulence of the C. glabrata Δire1 mutant in a mouse model of disseminated candidiasis. This study has unveiled the unique evolution of ER stress response mechanisms in C. glabrata. © 2013 Miyazaki et al. Source


Tashiro R.,Suzuka University of Medical Science | Ohtsuki A.,Kyoto University | Sugiyama H.,Kyoto University
Journal of the American Chemical Society | Year: 2010

We have investigated the products of BrU in excess electron transfer and have demonstrated that in DNA the proportion of products changes with the distance between the donor and acceptor. On the basis of a labeling experiment using H2 18O, we have shown that hole migration from Py•+ formed after charge separation is involved in the reaction. © 2010 American Chemical Society. Source

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