Evidence map›Paper›PMID 30653406›Full record

ArticleAutophagy2019

Skeletal muscle-specific Prmt1 deletion causes muscle atrophy via deregulation of the PRMT6-FOXO3 axis.

Seri Choi, Hyeon-Ju Jeong, Hyebeen Kim, Dahee Choi, Sung-Chun Cho, Je Kyung Seong, Seung-Hoi Koo, Jong-Sun Kang

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

78 citing papers in PubMed, 128 citations in OpenAlex.

  1. Dysregulated mScience advances · 2026
    Article
  2. Review
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  17. Article
  18. Lysine and arginine methylation of transcription factors.Cellular and molecular life sciences : CMLS · 2024
    Review
  19. Targeting ROS in cancer: rationale and strategies.Nature reviews. Drug discovery · 2024
    Review
  20. Epigenetics of Skeletal Muscle Atrophy.International journal of molecular sciences · 2024
    Review

18 more citing papers are in PubMed but not listed here.

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

8 authors at 5 institutions in 1 country.

Seri Choia Division of Life Sciences , Korea University , Seoul , South Korea.
Hyeon-Ju Jeongb Department of Molecular Cell Biology, Single Cell Network Research Center , Sungkyunkwan University School of Medicine , Suwon , South Korea.
Hyebeen Kimb Department of Molecular Cell Biology, Single Cell Network Research Center , Sungkyunkwan University School of Medicine , Suwon , South Korea.
Dahee Choia Division of Life Sciences , Korea University , Seoul , South Korea.
Sung-Chun Choc Well Aging Research Center, Samsung Advanced Institute of Technology , Samsung Electronics Co. Ltd , Suwon , South Korea.
Je Kyung Seongd Korea Mouse Phenotyping Center , Seoul National University , Seoul , South Korea.
Seung-Hoi Kooa Division of Life Sciences , Korea University , Seoul , South Korea.
Jong-Sun Kangb Department of Molecular Cell Biology, Single Cell Network Research Center , Sungkyunkwan University School of Medicine , Suwon , South Korea.
Korea University · KRSungkyunkwan University · KRSamsung Medical Center · KRSamsung (South Korea) · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein arginine methyltransferases (PRMTs) have emerged as important regulators of skeletal muscle metabolism and regeneration. However, the direct roles of the various PRMTs during skeletal muscle remodeling remain unclear. Using skeletal muscle-specific prmt1 knockout mice, we examined the function and downstream targets of PRMT1 in muscle homeostasis. We found that muscle-specific PRMT1 deficiency led to muscle atrophy. PRMT1-deficient muscles exhibited enhanced expression of a macroautophagic/autophagic marker LC3-II, FOXO3 and muscle-specific ubiquitin ligases, TRIM63/MURF-1 and FBXO32, likely contributing to muscle atrophy. The mechanistic study reveals that PRMT1 regulates FOXO3 through PRMT6 modulation. In the absence of PRMT1, increased PRMT6 specifically methylates FOXO3 at arginine 188 and 249, leading to its activation. Finally, we demonstrate that PRMT1 deficiency triggers FOXO3 hyperactivation, which is abrogated by PRMT6 depletion. Taken together, PRMT1 is a key regulator for the PRMT6-FOXO3 axis in the control of autophagy and protein degradation underlying muscle maintenance. Abbreviations: Ad-RNAi: adenovirus-delivered small interfering RNA; AKT: thymoma viral proto-oncogene; AMPK: AMP-activated protein kinase; Baf A1: bafilomycin A

Indexed as

AnimalsAutophagyForkhead Box Protein O3HEK293 CellsHistone Deacetylase 2Histone Deacetylase 3Histone DeacetylasesHumansMethylationMiceMice, KnockoutMicrotubule-Associated ProteinsMuscle ProteinsMuscle, SkeletalMuscular AtrophyPhosphorylationForkhead Box Protein O3FoxO3 protein, mouseHdac2 protein, mouseHistone Deacetylase 2Histone Deacetylase 3Histone DeacetylasesMap1lc3b protein, mouseMAS1 protein, humanMicrotubule-Associated ProteinsMuscle ProteinsPrmt1 protein, mousePRMT6 protein, mouseProtein-Arginine N-MethyltransferasesProto-Oncogene MasTrim63 protein, mouseTripartite Motif ProteinsUbiquitin-Protein LigasesYy1 protein, mouseYY1 Transcription FactorArginine methylationFOXO3muscle atrophyPRMT1PRMT6

Identifiers

PMID30653406
PMCPMC6526864
OpenAlexW2908751660

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.