Evidence map›Paper›PMID 40258148›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2025

MOB1 deletion in murine mature adipocytes ameliorates obesity and diabetes.

Miki Nishio, Keiko Yamaguchi, Junji Otani, Katsuya Yuguchi, Daisuke Kohno, Tsutomu Sasaki, Tadahiro Kitamura, Masakazu Shinohara, Tomoyoshi Soga, Koichi Kawamura and 9 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

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

19 authors.

Miki Nishio *Division of Molecular and Cellular Biology, Kobe University Graduate School of Medicine, Kobe, Hyogo 650-0017, Japan.
Keiko Yamaguchi *Division of Molecular and Cellular Biology, Kobe University Graduate School of Medicine, Kobe, Hyogo 650-0017, Japan.
Junji Otani *Division of Molecular and Cellular Biology, Kobe University Graduate School of Medicine, Kobe, Hyogo 650-0017, Japan.
Katsuya YuguchiDivision of Molecular and Cellular Biology, Kobe University Graduate School of Medicine, Kobe, Hyogo 650-0017, Japan.
Daisuke KohnoMetabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma 371-8512, Japan.ORCID 0009-0001-1073-2745
Tsutomu SasakiMetabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma 371-8512, Japan.ORCID 0000-0001-8041-1915
Tadahiro KitamuraMetabolic Signal Research Center, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma 371-8512, Japan.ORCID 0000-0001-8809-8740
Masakazu ShinoharaDivision of Molecular Epidemiology, Kobe University Graduate School of Medicine, Kobe, Hyogo 650-0017, Japan.
Tomoyoshi SogaInstitute for Advanced Biosciences, Keio University, Tsuruoka, Yamagata 997-0052, Japan.ORCID 0000-0001-9502-2509
Koichi KawamuraFaculty of Science and Engineering, Waseda University, Tokyo 162-0056, Japan.
Atsuo T SasakiInstitute for Advanced Biosciences, Keio University, Tsuruoka, Yamagata 997-0052, Japan.ORCID 0000-0003-2963-4501
Masashi OshimaDivision of Hematology and Oncology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH 45267.
Hiroki HikasaDepartment of Biochemistry, School of Medicine, University of Occupational and Environmental Health, Fukuoka 807-8555, Japan.
Minna WooBanting and Best Diabetes Centre, University of Toronto, Toronto, ON M5G 2C4, Canada.
Takehiko SasakiMedical Research Laboratory, Institute of Integrated Research, Institute of Science Tokyo, Tokyo 113-8510, Japan.
Hiroshi NishinaMedical Research Laboratory, Institute of Integrated Research, Institute of Science Tokyo, Tokyo 113-8510, Japan.
Kazuwa NakaoMedical Innovation Center, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan.
Tomohiko MaehamaDivision of Molecular and Cellular Biology, Kobe University Graduate School of Medicine, Kobe, Hyogo 650-0017, Japan.
Akira SuzukiDivision of Molecular and Cellular Biology, Kobe University Graduate School of Medicine, Kobe, Hyogo 650-0017, Japan.ORCID 0000-0002-5950-8808

Funding

Mechanistic role of phosphatidylinositol 5-phosphate 4-kinase beta in GTP-dependent lysosomal acidification for stress-resilient cell growth and metabolismR01GM144426 · NIGMS · UNIVERSITY OF CINCINNATI · PI Atsuo Sasaki · 2023 to 2026
$1.7M
Foundation for the National Institutes of Health (FNIH) R01GM144426Japan Agency for Medical Research and Development (AMED) 23ama221117h0002Japan Agency for Medical Research and Development (AMED) 24gm1710007s0102Japan Agency for Medical Research and Development (AMED) JP21zf0127001MEXT | Japan Society for the Promotion of Science (JSPS) 17H01400MEXT | Japan Society for the Promotion of Science (JSPS) 21H04806MEXT | Japan Society for the Promotion of Science (JSPS) 23H04946MEXT | Japan Society for the Promotion of Science (JSPS) 23K06400MEXT | Japan Society for the Promotion of Science (JSPS) 23K08009MEXT | Japan Society for the Promotion of Science (JSPS) 24K01941MEXT | JST | Core Research for Evolutional Science and Technology (CREST) JPMJCR2123Ministry of Education, Culture, Sports, Science and Technology (MEXT) Human Biology-Microbiome-Quantum Research CenterMinistry of Education, Culture, Sports, Science and Technology (MEXT) World Premier International Research Center InitiativeNIGMS NIH HHS R01 GM144426Scientific Research on Innovative Areas 25126719Tokyo Medical and Dental University (TMDU) Nanken-Kyoten
6 · The paper itself

Abstract

There is currently a global epidemic of obesity and obesity-related diseases such as type 2 diabetes due to decreased physical activity, excessive food intake, and/or genetic predisposition. The Hippo-YAP1 pathway has attracted attention as a potential therapeutic target because YAP1/TAZ activation in murine immature adipocytes in vitro suppresses their differentiation by inhibiting PPARγ activity. However, the role of YAP1 activation in mature adipocytes in vivo remains unclear. MOB1, whose expression is increased in obesity, is the hub of the Hippo core molecule complex and negatively regulates YAP1/TAZ activation. Therefore, we generated aMob1DKO mutant mice, which feature deficiency of

Indexed as

Adaptor Proteins, Signal TransducingAdipocytesDiabetes Mellitus, Type 2ObesityAdipose Tissue, WhiteAnimalsDiet, High-FatEnergy MetabolismFibroblast Growth FactorsInsulin ResistanceLipolysisMaleMiceMice, Inbred C57BLMice, KnockoutYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingFibroblast Growth FactorsYap1 protein, mouseYAP-Signaling ProteinsadipocytesdiabetesMOB1-YAP1-FGF21-OPA1 axisobesity

Identifiers

PMID40258148
PMCPMC12054810

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.