Evidence map›Paper›PMID 37474791›Full record

ArticleNature aging2023

LONRF2 is a protein quality control ubiquitin ligase whose deficiency causes late-onset neurological deficits.

Dan Li, Yoshikazu Johmura, Satoru Morimoto, Miyuki Doi, Keiko Nakanishi, Manabu Ozawa, Yuji Tsunekawa, Akane Inoue-Yamauchi, Hiroya Naruse, Takashi Matsukawa and 21 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% of its field
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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Cellular senescence as a source of chronic microinflammation that promotes the aging process.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2025
    Review
  4. Article
  5. Review
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

31 authors at 9 institutions in 1 country.

Dan LiDivision of Cancer Cell Biology, The University of Tokyo, Tokyo, Japan.
Yoshikazu JohmuraDivision of Cancer Cell Biology, The University of Tokyo, Tokyo, Japan. johmuray@staff.kanazawa-u.ac.jp.ORCID http://orcid.org/0000-0002-6812-9607
Satoru MorimotoDepartment of Physiology, Keio University School of Medicine, Tokyo, Japan.
Miyuki DoiDepartment of Neuroscience and Cell Biology, Osaka University Graduate School of Medicine, Osaka, Japan.
Keiko NakanishiDepartment of Pediatrics, Central Hospital, and Department of Disease Model, Institute for Developmental Research, Aichi Developmental Disability Center, Kasugai, Japan.
Manabu OzawaLaboratory of Reproductive Systems Biology, The University of Tokyo, Tokyo, Japan.
Yuji TsunekawaDivision of Molecular and Medical Genetics, Center for Gene and Cell Therapy, The University of Tokyo, Tokyo, Japan.
Akane Inoue-YamauchiDivision of Genetics, The University of Tokyo, Tokyo, Japan.
Hiroya NaruseDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-1190-0499
Takashi MatsukawaDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yukio TakeshitaDepartment of Neurology and Clinical Neuroscience, Yamaguchi University Graduate School of Medicine, Yamaguchi, Japan.ORCID http://orcid.org/0000-0002-0314-550X
Naoki SuzukiDepartment of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan.ORCID http://orcid.org/0000-0001-8880-8554
Masashi AokiDepartment of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Ayumi NishiyamaDepartment of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Xin ZengLaboratory of Functional Analysis in silico, Human Genome Center, The University of Tokyo, Tokyo, Japan.
Chieko KonishiDivision of Cancer Cell Biology, The University of Tokyo, Tokyo, Japan.
Narumi SuzukiDivision of Cancer Cell Biology, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0001-6024-9949
Atsuya NishiyamaDivision of Cancer Cell Biology, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-8416-3776
Alexander Stephen HarrisDivision of Cancer Cell Biology, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0009-0003-1005-3691
Mariko MoritaDivision of Clinical Genome Research, The University of Tokyo, Tokyo, Japan.
Kiyoshi YamaguchiDivision of Clinical Genome Research, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0003-2113-4369
Yoichi FurukawaDivision of Clinical Genome Research, The University of Tokyo, Tokyo, Japan.
Kenta NakaiLaboratory of Functional Analysis in silico, Human Genome Center, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-8721-8883
Shoji TsujiDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0001-5602-5686
Satoshi YamazakiDivision of Stem Cell Biology, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0003-4249-3854
Yuji YamanashiDivision of Genetics, The University of Tokyo, Tokyo, Japan.
Shoichi ShimadaDepartment of Neuroscience and Cell Biology, Osaka University Graduate School of Medicine, Osaka, Japan.
Takashi OkadaDivision of Molecular and Medical Genetics, Center for Gene and Cell Therapy, The University of Tokyo, Tokyo, Japan.
Hideyuki OkanoDepartment of Physiology, Keio University School of Medicine, Tokyo, Japan.ORCID http://orcid.org/0000-0001-7482-5935
Tatsushi TodaDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-0717-1123
Makoto NakanishiDivision of Cancer Cell Biology, The University of Tokyo, Tokyo, Japan. mkt-naka@g.ecc.u-tokyo.ac.jp.ORCID http://orcid.org/0000-0002-6707-3584
The University of Tokyo · JPTohoku University · JPKeio University · JPThe University of Osaka · JPTokyo Medical University · JPAichi Developmental Disability Center · JPKanazawa University · JPUniversity of Tsukuba · JPYamaguchi University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein misfolding is a major factor of neurodegenerative diseases. Post-mitotic neurons are highly susceptible to protein aggregates that are not diluted by mitosis. Therefore, post-mitotic cells may have a specific protein quality control system. Here, we show that LONRF2 is a bona fide protein quality control ubiquitin ligase induced in post-mitotic senescent cells. Under unperturbed conditions, LONRF2 is predominantly expressed in neurons. LONRF2 binds and ubiquitylates abnormally structured TDP-43 and hnRNP M1 and artificially misfolded proteins. Lonrf2

Indexed as

Motor NeuronsUbiquitinUbiquitin-Protein LigasesAnimalsDNA-Binding ProteinsDNA HelicasesLigasesMicePoly-ADP-Ribose Binding ProteinsRNA HelicasesRNA Recognition Motif ProteinsDNA-Binding ProteinsDNA HelicasesLigasesLonrf2 protein, mousePoly-ADP-Ribose Binding ProteinsRNA HelicasesRNA Recognition Motif ProteinsUbiquitinUbiquitin-Protein Ligases

Identifiers

PMID37474791
OpenAlexW4384924934

What OpenQuestion holds

Textmetadata
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.