Author

Yuki Masujima

Kyoto University

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Physiology· 3

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:mouse· 3 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:development & morphogenesis· 1 Research Focus:host-pathogen & immune response· 1 Research Focus:metabolism & bioenergetics· 1

Frequent Co-Authors

Ikuo KimuraiD· 3 shared Mayu YamanoiD· 3 shared Akari NishidaiD· 2 shared Eiji KondohiD· 2 shared Fumitaka OsakadaiD· 2 shared Hiroaki OhnoiD· 2 shared Junken AokiiD· 2 shared Junki MiyamotoiD· 2 shared

Activity by Year

2025-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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3 shared papersPhysiology

Ikuo KimuraORCID

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3 papers

Recent·Most cited

Maternal progesterone signaling establishes lifelong oral homeostasis

Mayu Yamano, Junki Miyamoto, Daiki Sasahara, Yuki Masujima, Takako Ikeda, Ryuji Ohue‐Kitano, Akari Nishida, Shingo Kawai, Rina Kurokawa, Nozomu Kono, Munekage Yamaguchi, Shinsuke Inuki, Fumitaka Osakada, Kentaro Nagaoka, Hiroaki Ohno, , Ikuo Kimura

This study identifies maternal progesterone signaling through mPRδ as critical for establishing lifelong oral homeostasis via a hormone-lipid-microbiome axis.

bioRxiv · Aug 19, 2026 · PreprintPhysiology

Maternal progesterone and adipose mPRε in pregnancy regulate the embryonic nutritional state

Keita Watanabe, Mayu Yamano, Junki Miyamoto, Ryuji Ohue‐Kitano, Yuki Masujima, Daiki Sasahara, Yuki Mouri, Nozomu Kono, Shunsuke Inuki, Fumitaka Osakada, Kentaro Nagaoka, Junken Aoki, Yuki Sugiura, Hiroaki Ohno, Eiji Kondoh, Ikuo Kimura

This study shows that maternal progesterone and adipose mPRε regulate the embryonic nutritional state by affecting glucose provision and metabolic outcomes in offspring.

Cell Reports · Mar 1, 2025Peer-reviewedPhysiology

The pivotal role of a novel free fatty acid receptor GPR164 in the intestinal barrier function

Takako Ikeda, Yuki Masujima, Keita Watanabe, Akari Nishida, Mayu Yamano, Miki Igarashi, Nobuo Sasaki, Hironori Katoh, Ikuo Kimura

This study shows that GPR164 deletion in mice causes intestinal barrier dysfunction, Wnt/β-catenin signaling disruption, and IBD-like symptoms, suggesting GPR164 as a therapeutic target for IBD.

bioRxiv · Feb 20, 2025 · PreprintPhysiology