Evidence map›Paper›PMID 36309524›Full record

ArticleNature communications2022

Glutamyl-prolyl-tRNA synthetase 1 coordinates early endosomal anti-inflammatory AKT signaling.

Eun-Young Lee, Su-Man Kim, Jung Hwan Hwang, Song Yee Jang, Shinhye Park, Sanghyeon Choi, Ga Seul Lee, Jungwon Hwang, Jeong Hee Moon, Paul L Fox and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
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  10. AKT-dependent nuclear localization of EPRS1 activates PARP1 in breast cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  11. Article
  12. Review
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

13 authors at 3 institutions in 2 countries.

Eun-Young LeeMicrobiome Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Korea. krupi00@kribb.re.kr.ORCID 0000-0003-3120-9192
Su-Man KimMicrobiome Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Korea.ORCID 0000-0002-0588-8294
Jung Hwan HwangLaboratory Animal Resource Center, KRIBB, Daejeon, 34141, Korea.
Song Yee JangMicrobiome Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Korea.
Shinhye ParkMicrobiome Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Korea.
Sanghyeon ChoiMicrobiome Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Korea.
Ga Seul LeeCore Research Facility & Analysis Center, KRIBB, Daejeon, 34141, Korea.
Jungwon HwangMicrobiome Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Korea.ORCID 0000-0002-4628-6177
Jeong Hee MoonCore Research Facility & Analysis Center, KRIBB, Daejeon, 34141, Korea.
Paul L FoxDepartment of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH, 44195, USA.
Sunghoon KimMedicinal Bioconvergence Research Center, College of Pharmacy and College of Medicine, Gangnam Severance Hospital, Yonsei University, Incheon, 21983, Korea.ORCID 0000-0002-1570-3230
Chul-Ho LeeLaboratory Animal Resource Center, KRIBB, Daejeon, 34141, Korea.ORCID 0000-0002-6996-5746
Myung Hee KimMicrobiome Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, 34141, Korea. mhk8n@kribb.re.kr.ORCID 0000-0003-2856-9066
Korea Research Institute of Bioscience and Biotechnology · KRYonsei University · KRCleveland Clinic · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The AKT signaling pathway plays critical roles in the resolution of inflammation. However, the underlying mechanisms of anti-inflammatory regulation and signal coordination remain unclear. Here, we report that anti-inflammatory AKT signaling is coordinated by glutamyl-prolyl-tRNA synthetase 1 (EPRS1). Upon inflammatory activation, AKT specifically phosphorylates Ser999 of EPRS1 in the cytoplasmic multi-tRNA synthetase complex, inducing release of EPRS1. EPRS1 compartmentalizes AKT to early endosomes via selective binding to the endosomal membrane lipid phosphatidylinositol 3-phosphate and assembles an AKT signaling complex specific for anti-inflammatory activity. These events promote AKT activation-mediated GSK3β phosphorylation, which increase anti-inflammatory cytokine production. EPRS1-deficient macrophages do not assemble the early endosomal complex and consequently exacerbate inflammation, decreasing the survival of EPRS1-deficient mice undergoing septic shock and ulcerative colitis. Collectively, our findings show that the housekeeping protein EPRS1 acts as a mediator of inflammatory homeostasis by coordinating compartment-specific AKT signaling.

Indexed as

Proto-Oncogene Proteins c-aktSignal TransductionAmino Acyl-tRNA SynthetasesAnimalsAnti-Inflammatory AgentsInflammationMiceAmino Acyl-tRNA SynthetasesAnti-Inflammatory Agentsglutamyl-prolyl-tRNA synthetaseProto-Oncogene Proteins c-akt

Identifiers

PMID36309524
PMCPMC9617928
OpenAlexW4307844981

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.