K
Koji Ueda
Researcher at Japanese Foundation for Cancer Research
Publications - 136
Citations - 3077
Koji Ueda is an academic researcher from Japanese Foundation for Cancer Research. The author has contributed to research in topics: Cancer & Medicine. The author has an hindex of 29, co-authored 101 publications receiving 2370 citations. Previous affiliations of Koji Ueda include Institute of Medical Science & University of Tokyo.
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Antibody-coupled monolithic silica microtips for highthroughput molecular profiling of circulating exosomes
TL;DR: A simple anti-CD9 antibody-coupled highly porous monolithic silica microtips are constructed which allowed automated rapid and reproducible exosome extraction from multiple clinical samples and can promote not only biomarker discovery studies but also wide range of omics researches about exosomes.
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Histone Lysine Methyltransferase SETD8 Promotes Carcinogenesis by Deregulating PCNA Expression
Masashi Takawa,Hyun-Soo Cho,Shinya Hayami,Gouji Toyokawa,Masaharu Kogure,Masaharu Kogure,Yuka Yamane,Yukiko Iwai,Kazuhiro Maejima,Koji Ueda,Akiko Masuda,Naoshi Dohmae,Helen I. Field,Tatsuhiko Tsunoda,Takaaki Kobayashi,Takayuki Akasu,Masanori Sugiyama,Shin Ichi Ohnuma,Yutaka Atomi,Bruce A.J. Ponder,Yusuke Nakamura,Yusuke Nakamura,Ryuji Hamamoto,Ryuji Hamamoto +23 more
TL;DR: It is shown that SETD8 regulates the function of proliferating cell nuclear antigen (PCNA) protein through lysine methylation, and an increase of methylated PCNA was found in cancer cells, and the expression levels ofSETD8 and PCNA were correlated in cancer tissue samples, suggesting that aberrant lysines methylation of PCNA may play a role in human carcinogenesis.
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Exosomal microRNA miR-1246 induces cell motility and invasion through the regulation of DENND2D in oral squamous cell carcinoma
TL;DR: It is demonstrated that exosomes isolated by size-exclusion chromatography from a highly metastatic human oral cancer cell line, HOC313-LM, induced cell growth through the activation of ERK and AKT as well as promoted cell motility of the poorly metastaticcancer cell line HOC 313-P.
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Development of an orally-administrative MELK-targeting inhibitor that suppresses the growth of various types of human cancer.
Suyoun Chung,Hanae Suzuki,Takashi Miyamoto,Naofumi Takamatsu,Ayako Tatsuguchi,Koji Ueda,Kyoko Kijima,Yusuke Nakamura,Yo Matsuo +8 more
TL;DR: A high-throughput screening of a compound library followed by structure-activity relationship studies, and successfully obtained a highly potent MELK inhibitor OTSSP167 with IC50 of 0.41 nM, which should be a promising compound possibly to suppress the growth of tumor-initiating cells and be applied for treatment of a wide range of human cancer.
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Regulation of histone modification and chromatin structure by the p53–PADI4 pathway
Chizu Tanikawa,Martha Espinosa,Akari Suzuki,Ken Masuda,Kazuhiko Yamamoto,Eiju Tsuchiya,Koji Ueda,Yataro Daigo,Yataro Daigo,Yusuke Nakamura,Koichi Matsuda +10 more
TL;DR: In vivo and in vitro citrullination of the arginine 3 residue of histone H4 (cit-H4R3) in response to DNA damage through the p53-PADI4 pathway is shown and reveals that cit-H 4R3 may be an 'apoptotic histone code' to detect damaged cells and induce nuclear fragmentation, which has a crucial role in carcinogenesis.