Rchr
J-GLOBAL ID:201801005254469505
Update date: Feb. 01, 2024
Muramatsu Tomoki
ムラマツ トモキ | Muramatsu Tomoki
Affiliation and department:
Research field (1):
Molecular biology
Research theme for competitive and other funds (8):
- 2021 - 2024 Analysis of mechanisms of the hypoxic responses by BET proteins
- 2018 - 2021 Development of therapeutic miRNAs targeting BET family protein BRD4 for cancer
- 2018 - 2020 Exploring the transcriptional repressors of VEGFA by in vitro/in vivo high throughput screening
- 2015 - 2020 Establishment of novel concept for cancer diagnostics and therapeutics based on the systematic comprehension of cellular context in cancer
- 2015 - 2017 Analysis of mechanism of hypusine pathway in cancer
- 2013 - 2016 Comprehensive understanding of molecular carcinogenesis through omics analysis and development of molecular diagnostics for personalized medicine
- 2014 - 2015 新規がん治療標的経路として見出されたhypusine axisの分子機構の解明
- 2012 - 2013 上皮間葉転換を基軸としたがん転移能獲得機構の解明
Show all
Papers (29):
-
Chang Liu, Yasuyuki Gen, Kousuke Tanimoto, Tomoki Muramatsu, Jun Inoue, Johji Inazawa. Concurrent targeting of MAP3K3 and BRD4 by miR-3140-3p overcomes acquired resistance to BET inhibitors in neuroblastoma cells. Molecular Therapy - Nucleic Acids. 2021. 25. 83-92
-
Yasuyuki Gen, Tomoki Muramatsu, Jun Inoue, Johji Inazawa. miR-766-5p targets super-enhancers by downregulating CBP and BRD4. Cancer research. 2021
-
Koichi Nishino, Yasuhiro Yoshimatsu, Tomoki Muramatsu, Yasuhito Sekimoto, Keiko Mitani, Etsuko Kobayashi, Shouichi Okamoto, Hiroki Ebana, Yoshinori Okada, Masatoshi Kurihara, et al. Isolation and characterisation of lymphatic endothelial cells from lung tissues affected by lymphangioleiomyomatosis. Scientific reports. 2021. 11. 1. 8406-8406
-
Bo Xu, Tomoki Muramatsu, Johji Inazawa. Suppression of MET Signaling Mediated by Pitavastatin and Capmatinib Inhibits Oral and Esophageal Cancer Cell Growth. Molecular cancer research : MCR. 2020. 19. 4. 585-597
-
Elena Deryugina, Alexia Carré, Veronica Ardi, Tomoki Muramatsu, Jonas Schmidt, Christine Pham, James P Quigley. Neutrophil Elastase Facilitates Tumor Cell Intravasation and Early Metastatic Events. iScience. 2020. 23. 12. 101799-101799
more...
MISC (45):
-
村松 智輝, 徐 博, 稲澤 譲治. 口腔・食道がんにおいてピタバスタチンはAKT、ERKのシグナルを抑制し、細胞増殖を阻害する. 日本癌学会総会記事. 2020. 79回. OE5-8
-
内藤 諒, 村松 智輝, 谷本 幸介, 稲澤 譲治. 統合的mRNA, miRNA発現情報を基盤とした独自のマイクロRNA標的遺伝子予測データベースの構築(Construction of an in-house microRNA-target prediction database based on an integrative mRNA-microRNA expression data). 日本癌学会総会記事. 2019. 78回. E-1063
-
村松 智輝, 佐藤 拓, 田邉 稔, 稲澤 譲治. 循環腫瘍細胞亜株(Panc-1-CTC)の発現解析から見出したTGFBIの機能解析(Identification and characterization of TGFBI in circulating tumor cell subline from pancreatic cancer cell line). 日本癌学会総会記事. 2019. 78回. P-1058
-
高川 祐希, 玄 泰行, 村松 智輝, 原田 浩之, 稲澤 譲治. 機能的miRNAライブラリースクリーニングによる、BRD4を標的とする新規癌抑制型miRNAの同定(Function-based microRNA library screening identified novel tumor suppressive microRNAs targeting BRD4). 日本癌学会総会記事. 2019. 78回. P-1238
-
吉松 康裕, 赤津 裕一, 高橋 直也, 紀室 志織, 村松 智輝, 桂 彰宏, 間石 奈湖, 鈴木 洋, 稲澤 譲治, 樋田 京子, et al. 線維芽細胞増殖因子(FGF2)は腫瘍血管内皮細胞においてTGF-βによって誘導される内皮-筋線維芽移行を制御する(Fibroblast growth factor 2 regulates TGF-β-induced endothelial-to-myofibroblast transition of tumor endothelial cells). 日本癌学会総会記事. 2019. 78回. P-2280
more...
Lectures and oral presentations (34):
-
口腔・食道がんにおいてピタバスタチンはAKT、ERKのシグナルを抑制し、細胞増殖を阻害する
(日本癌学会総会記事 2020)
-
新規癌抑制型miRNAによるMYC標的核酸抗癌治療の可能性(Oligonucleotide therapeutics using a novel tumor-suppressive microRNA targeting MYC pathway)
(日本癌学会総会記事 2019)
-
扁平上皮がん細胞においてピタバスタチンはAKT、ERKの抑制を介して細胞増殖を阻害する(Pitavastatin inhibits the cell growth through the downregulation of AKT and ERK in squamous cell carcinoma)
(日本癌学会総会記事 2019)
-
線維芽細胞増殖因子(FGF2)は腫瘍血管内皮細胞においてTGF-βによって誘導される内皮-筋線維芽移行を制御する(Fibroblast growth factor 2 regulates TGF-β-induced endothelial-to-myofibroblast transition of tumor endothelial cells)
(日本癌学会総会記事 2019)
-
機能的miRNAライブラリースクリーニングによる、BRD4を標的とする新規癌抑制型miRNAの同定(Function-based microRNA library screening identified novel tumor suppressive microRNAs targeting BRD4)
(日本癌学会総会記事 2019)
more...
Association Membership(s) (2):
Return to Previous Page