Evidence map›Paper›PMID 26246171›Full record

ArticleNature communications2015

The mitochondrial ubiquitin ligase MARCH5 resolves MAVS aggregates during antiviral signalling.

Young-Suk Yoo, Yong-Yea Park, Jae-Hoon Kim, Hyeseon Cho, Song-Hee Kim, Ho-Soo Lee, Tae-Hwan Kim, You Sun Kim, Youngsoo Lee, Chul-Joong Kim and 3 more

Abstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing 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

107 citing papers in PubMed.

  1. Article
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  8. Review
  9. MARCH E3 Ligases: Understudied Regulators of Pulmonary Immune Function.Journal of respiratory biology and translational medicine · 2026
    Article
  10. Article
  11. Review
  12. Article
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47 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

13 authors.

Young-Suk Yoo1] Department of Biochemistry, Ajou University School of Medicine, Graduate School of Ajou University, Suwon 443-380, Korea [2] Department of Biological Sciences, Graduate School of Ajou University, Suwon 443-380, Korea.
Yong-Yea ParkDepartment of Biochemistry, Ajou University School of Medicine, Graduate School of Ajou University, Suwon 443-380, Korea.
Jae-Hoon KimCollege of Veterinary Medicine (BK21 Plus Program), Chungnam National University, Daejeon 305-764, Korea.
Hyeseon ChoMucosal Immunobiology Section, Laboratory of Molecular Immunology, NIAID, NIH, Bethesda, Maryland 20852, USA.
Song-Hee KimDepartment of Biochemistry, Ajou University School of Medicine, Graduate School of Ajou University, Suwon 443-380, Korea.
Ho-Soo Lee1] Department of Biochemistry, Ajou University School of Medicine, Graduate School of Ajou University, Suwon 443-380, Korea [2] Department of Biological Sciences, Graduate School of Ajou University, Suwon 443-380, Korea.
Tae-Hwan KimCollege of Veterinary Medicine (BK21 Plus Program), Chungnam National University, Daejeon 305-764, Korea.
You Sun Kim1] Department of Biochemistry, Ajou University School of Medicine, Graduate School of Ajou University, Suwon 443-380, Korea [2] Department of Biological Sciences, Graduate School of Ajou University, Suwon 443-380, Korea.
Youngsoo Lee1] Department of Biological Sciences, Graduate School of Ajou University, Suwon 443-380, Korea [2] Genomic Instability Research Center, Ajou University School of Medicine, Suwon 443-380, Korea.
Chul-Joong KimCollege of Veterinary Medicine (BK21 Plus Program), Chungnam National University, Daejeon 305-764, Korea.
Jae U JungDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, California 90089, USA.
Jong-Soo LeeCollege of Veterinary Medicine (BK21 Plus Program), Chungnam National University, Daejeon 305-764, Korea.
Hyeseong Cho1] Department of Biochemistry, Ajou University School of Medicine, Graduate School of Ajou University, Suwon 443-380, Korea [2] Department of Biological Sciences, Graduate School of Ajou University, Suwon 443-380, Korea [3] Genomic Instability Research Center, Ajou University School of Medicine, Suwon 443-380, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria serve as platforms for innate immunity. The mitochondrial antiviral signalling (MAVS) protein forms aggregates that elicit robust type-I interferon induction on viral infection, but persistent MAVS signalling leads to host immunopathology; it remains unknown how these signalling aggregates are resolved. Here we identify the mitochondria-resident E3 ligase, MARCH5, as a negative regulator of MAVS aggregates. March5(+/-) mice and MARCH5-deficient immune cells exhibit low viral replication and elevated type-I interferon responses to RNA viruses. MARCH5 binds MAVS only during viral stimulation when MAVS forms aggregates, and these interactions require the RING domain of MARCH5 and the CARD domain of MAVS. MARCH5, but not its RING mutant (MARCH5(H43W)), reduces the level of MAVS aggregates. MARCH5 transfers ubiquitin to Lys7 and Lys500 of MAVS and promotes its proteasome-mediated degradation. Our results indicate that MARCH5 modulates MAVS-mediated antiviral signalling, preventing excessive immune reactions.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsHEK293 CellsHumansImmunity, InnateInterferon Type IMembrane ProteinsMice, Inbred C57BLMitochondriaMitochondrial ProteinsRNA Virus InfectionsUbiquitinUbiquitin-Protein LigasesAdaptor Proteins, Signal TransducingInterferon Type IMARCHF5 protein, humanMarchf5 protein, mouseMAVS protein, humanMAVS protein, mouseMembrane ProteinsMitochondrial ProteinsUbiquitinUbiquitin-Protein Ligases

Identifiers

PMID26246171
PMCPMC4918326

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Registered trials

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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.