森脇一将

Moriwaki Kazumasa

所属機関・部署：
職名：講師

研究分野 (2件)：腫瘍生物学 , 病態医化学

研究キーワード (7件)：患者由来がんモデル , 癌転移 , 細胞接着 , 細胞運動 , 糖鎖 , 癌治療 , 希少がん

競争的資金等の研究課題 (7件)：

全件表示

論文 (23件)：

Makoto Shirakawa, Shunichi Yokoe, Takatoshi Nakagawa, Kazumasa Moriwaki, Toshihisa Takeuchi, Michio Asahi. Rapamycin and Starvation Mitigate Indomethacin-Induced Intestinal Damage through Preservation of Lysosomal Vacuolar ATPase Integrity. The Journal of pharmacology and experimental therapeutics. 2024. 390. 1. 108-115
Kazumasa Moriwaki, Yusuke Ayani, Hiroko Kuwabara, Tetsuya Terada, Masaaki Higashino, Ryo Kawata. Differential expression of TRKB tyrosine kinase in the two histological types of parotid salivary duct carcinoma with cancer aggressiveness. Oral Oncology. 2024. 151. 106751
Shigeaki Muto, Kazumasa Moriwaki, Daisuke Nagata, Mikio Furuse. Axial heterogeneity of superficial proximal tubule paracellular transport in mice (2024/10/27 Accepted). American Journal of Physiology-Renal Physiology. 2024
Natsuko MORITA, Hirofumi MORIHARA, Kazumasa MORIWAKI, Atsushi DAIMON, Michio ASAHI, Masahide OHMICHI. Intravenous Injection of iPS Cell-Derived Endothelial Progenitor Cells Prevents Miscarriage by Releasing Pro-Angiogenic Factors in a Mouse Model of Recurrent Spontaneous Abortion. Bulletin of Osaka Medical and Pharmaceutical University. 2023. 69. 1,2. 21-30
Mahito Matsuno, Shunichi Yokoe, Takehiro Nagatsuka, Hirofumi Morihara, Kazumasa Moriwaki, Michio Asahi. O-GlcNAcylation-induced GSK-3β activation deteriorates pressure overload-induced heart failure via lack of compensatory cardiac hypertrophy in mice. Frontiers in Endocrinology. 2023. 14

MISC (29件)：

上田康裕, 森脇一将, 小嶋融一, 竹内利寿, 朝日通雄, 樋口和秀. 消化管におけるtranslational research O-GlcNAc修飾はFOXM1を安定化することで癌の進展に働く. 日本消化管学会雑誌. 2021. 5. Suppl. 169-169
森脇一将, 上田康裕, 樋口和秀, 朝日通雄. O-GlcNAc修飾上昇はFBXL2によるFOXM1のポリユビキチン化を抑制してFOXM1を増加させる. 日本癌学会学術総会抄録集(Web). 2019. 78回. E-1026
Yasuhiro Ueda, Kazumasa Moriwaki, Noriaki Sugawara, Masanobu Fukumoto, Satoshi Harada, Kazuhiro Ota, Yuichi Kojima, Toshihisa Takeuchi, Kazuhide Higuchi, Michio Asahi. ELEVATED O-GLCNACYLATION INCREASES FOXM1 PROTEIN VIA SUPPRESSION OF ITS POLY-UBIQUITINATION AND SUBSEQUENT PROTEASOMAL DEGRADATION. GASTROENTEROLOGY. 2019. 156. 6. S1091-S1091
森脇一将, 上田康裕, 樋口和秀, 朝日通雄. O-GlcNAc修飾の上昇はFOXM1タンパクのプロテアソームでの分解を抑制してその発現を安定化している(Elevated O-GlcNAcylation stabilizes FOXM1 protein via suppression of its proteasomal degradation). 日本癌学会総会記事. 2018. 77回. 2124-2124
綾仁悠介, 森脇一将, 桑原宏子, 寺田哲也, 河田了, 朝日通雄. BDNF/TRKBシグナルは低分化型口腔扁平上皮癌治療の標的候補である(Therapeutic potential of targeting BDNF/TRKB signaling in poorly differentiated oral squamous cell carcinomas). 日本癌学会総会記事. 2018. 77回. 535-535

書籍 (3件)：

講演・口頭発表等 (59件)：

Intercellular crosstalk between patient-derived parotid gland cancer cells and CAFs via the BDNF/TRKB pathway
(日本患者由来がんモデル学会・日本ヒト細胞学会合同学術集会2024 2024)
Elevated O-GlcNAcylation in TME enhances metastasis of PAN02 pancreatic adenocarcinoma
(第82回日本癌学会学術総会(横浜) 2023)
The BDNF/TRKB pathway promotes EMT to induce parotid gland cancer cell aggressiveness via interaction with CAF
(第96回日本薬理学会年会 2022)
The BDNF/TRKB pathway promotes EMT to enhance parotid gland cancer cell aggressiveness via cross-talk with CAFs
(第81回日本癌学会学術総会 2022)
BDNF/TRKB axis provokes EMT progression to induce cell aggressiveness via cross-talk with cancer associated fibroblasts in human parotid gland cancer
(第95回日本薬理学会年会 2022)

学位 (2件)：

経歴 (2件)：

委員歴 (2件)：

受賞 (2件)：

2022/11 - 第96回日本薬理学会年会優秀ポスター賞 The BDNF/TRKB pathway promotes EMT to induce parotid gland cancer cell aggressiveness via interaction with CAF
2013/05 - 第60回日本生化学会近畿支部例会優秀発表賞腸管上皮細胞のバリア機能を調節する機能阻害抗体の作製

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森脇 一将