Article in EMBO reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
9 authors.
Takako IkedaLaboratory of Molecular Neurobiology, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto, 606-8501, Japan. ikeda.takako.2r@kyoto-u.ac.jp.ORCID 0000-0003-2068-1213
Yuki MasujimaLaboratory of Molecular Neurobiology, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto, 606-8501, Japan.
Keita WatanabeLaboratory of Molecular Neurobiology, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto, 606-8501, Japan.
Akari NishidaDepartment of Molecular Endocrinology, Graduate School of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto, 606-8501, Japan.
Mayu YamanoDepartment of Molecular Endocrinology, Graduate School of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto, 606-8501, Japan.
Miki IgarashiDepartment of Immunoregulation Institute of Medical Science, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, Tokyo, 160-8402, Japan.
Nobuo SasakiLaboratory of Mucosal Ecosystem Design, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Japan.
Hironori KatohDepartment of Biological Chemistry, Graduate School of Science, Osaka Metropolitan University, Gakuen-cho, Naka-ku, Sakai, Osaka, 599-8531, Japan.ORCID 0000-0002-8191-8117
Ikuo KimuraLaboratory of Molecular Neurobiology, Graduate School of Biostudies, Kyoto University, Sakyo-ku, Kyoto, 606-8501, Japan. kimura.ikuo.7x@kyoto-u.ac.jp.ORCID 0000-0001-8778-145X
Funding
Japan Agency for Medical Research and Development (AMED) JP23gm1510011 to I.K.MEXT | Japan Society for the Promotion of Science (JSPS) 22K21208MEXT | Japan Society for the Promotion of Science (JSPS) 23K16794MEXT | Japan Society for the Promotion of Science (JSPS) 25K21072MEXT | Japan Society for the Promotion of Science (JSPS) JP25H01097 to I.K.MEXT | JST | Moonshot Research and Development Program (Moonshot) JPMJMS2023
6 · The paper itself
Abstract
GPR164 is a free fatty acid receptor, activated by both short-chain fatty acids and medium-chain fatty acids, and expressed throughout the gastrointestinal tract. Although GPR164 is reported to be involved in the release of gut hormones, the physiological functions of this receptor in the maintenance of intestinal homeostasis remain unclear. In this study, we explore the role of GPR164 in regulating intestinal barrier function using mice lacking Gpr164 gene (Gpr164
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.
The free fatty acid receptor GPR164 maintains intestinal homeostasis and barrier function. · full record | Socratic