西川 毅
| 薬学部 薬学科 | 准教授 |
Last Updated :2025/06/19
■プロフィール情報
■業績リスト
論文
- Cloning of cDNA for cathepsin B mRNA 3'-untranslated-region-binding protein(CBBP),and characterization of recombinant CBBP.
We isolated a cDNA for cathepsin B mRNA 3'-untranslated-region-binding protein (CBBP) and showed that it contained RNA binding motifs such as RGG box and zinc finger motif., J.Biochem.129(3), 2001年03月, 有り - Targeted disruption of a pupal hemocyte protein of Sarcophaga by RNA interference.
共著, RNA interference was found to be a useful technique for silencing the expression of a specific gene in pupal hemocytes of Sarcophaga., Eur.J.Biochem.268(20), 2001年10月, 有り - Correlation between the catalase level in tumor cells and their sensitivity to N-β-alanyl-5-S-glutathionyl-3,4-dihydroxyphenylalanine (5-S-GAD).
共著, We demonstrated that the cellular catalase level was crucial for cell sensitivity to 5-S-GAD, an anti-tumor substance derived from insect., J.Biochem.135(4), 2004年04月, 有り - Inhibition of in vivo angiogenesis by N-β-alanyl-5-S-glutathionyl-3,4-dihydroxyphenylalanine.
共著, We showed that 5-S-GAD inhibited tumor cell-induced angiogenesis. 5-S-GAD also inhibited vascular endothelial growth factor-induced angiogenesis and embryonic angiogenesis., Eur.J.Phrmacol.539(3), 2006年04月, 有り - A long-lived o-semiquinone radical anion is formed from N-β-alanyl-5-S-glutathionyl-3,4-dihydroxyphenylalanine(5-S-GAD),an insect-derived antibacterial substance.
共著, We found that an o-semiquinone radical anion was formed from 5-S-GAD. This radical formation is involved in the production of hydrogen peroxide from 5-S-GAD., J.Biochem.142(1), 2007年07月, 有り
その他研究業績
- 細胞死誘導抗体を分泌するビフィズス菌を利用したがん治療
共著, 2015年03月, 日本薬学会第135年会（神戸）, We showed that intravenous administration of anaerobic Bifidobacteria secreting tetravalent VHHs targeting death receptor 5 (TRAIL-R2) suppressed the tumor growth in tumor-bearing mice. - TRAIL-R1を標的とした新規3価VHH抗体を分泌するビフィズス菌によるがん治療
共著, 2016年03月, 日本薬学会第136年会（横浜）（講演ハイライト選定）, We showed that intravenous administration of anaerobic Bifidobacteria secreting novel trivalent VHHs targeting death receptor 4 (TRAIL-R1) suppressed the tumor growth in tumor-bearing mice.
