Evidence map›Paper›PMID 30001419›Full record

ArticlePloS one2018

MARCH1-mediated ubiquitination of MHC II impacts the MHC I antigen presentation pathway.

Kayla R Wilson, Haiyin Liu, Geraldine Healey, Vivian Vuong, Satoshi Ishido, Marco J Herold, Jose A Villadangos, Justine D Mintern

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

29 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Review
  3. Broad systemic T cell immunity toFrontiers in immunology · 2026
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  6. Review
  7. CD83 suppresses endogenous March-I-dependent MHC class II ubiquitination, endocytosis, and degradation.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. IL-6-Driven Autocrine Lactate Promotes Immune Escape of Uveal Melanoma.Investigative ophthalmology & visual science · 2024
    Article
  17. Article
  18. Article
  19. Review
  20. 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

8 authors at 2 institutions in 2 countries.

Kayla R WilsonDepartment of Biochemistry and Molecular Biology, The University of Melbourne, Bio21 Molecular Science and Biotechnology Institute, Parkville, Victoria, Australia.
Haiyin LiuDepartment of Biochemistry and Molecular Biology, The University of Melbourne, Bio21 Molecular Science and Biotechnology Institute, Parkville, Victoria, Australia.
Geraldine HealeyDepartment of Biochemistry and Molecular Biology, The University of Melbourne, Bio21 Molecular Science and Biotechnology Institute, Parkville, Victoria, Australia.
Vivian VuongDepartment of Biochemistry and Molecular Biology, The University of Melbourne, Bio21 Molecular Science and Biotechnology Institute, Parkville, Victoria, Australia.
Satoshi IshidoDepartment of Microbiology, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Japan.
Marco J HeroldWalter and Eliza Hall Institute, Parkville, Victoria, Australia.
Jose A VilladangosDepartment of Biochemistry and Molecular Biology, The University of Melbourne, Bio21 Molecular Science and Biotechnology Institute, Parkville, Victoria, Australia.
Justine D MinternDepartment of Biochemistry and Molecular Biology, The University of Melbourne, Bio21 Molecular Science and Biotechnology Institute, Parkville, Victoria, Australia.ORCID 0000-0002-3797-8577
The University of Melbourne · AUHyogo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Major histocompatibility complex class II (MHC II) expression and turn-over are regulated via its ubiquitination by the membrane associated RING-CH 1 (MARCH1) E3 ligase. Unexpectedly, we show that MHC II ubiquitination also impacts MHC I. Lack of MARCH1 in B cells and dendritic cells (DCs) resulted in a significant reduction in surface MHC I expression. This decrease was not directly caused by changes in MARCH1 ubiquitination of MHC I but indirectly by altered MHC II trafficking in the absence of its ubiquitination. Deletion of MHC II in March1-/- cells restored normal MHC I surface expression and replacement of wild type MHC II by a variant that could not be ubiquitinated caused a reduction in MHC I expression. Furthermore, these cells displayed inefficient presentation of peptide and protein antigen via MHC I to CD8+ T cells. In summary, we describe an unexpected intersection between MHC I and MHC II such that the surface expression of both molecules are indirectly and directly regulated by MARCH1 ubiquitination, respectively.

Indexed as

AnimalsAntigen PresentationB-LymphocytesCD8-Positive T-LymphocytesCell LineDendritic CellsGene DeletionGene Expression RegulationHistocompatibility Antigens Class IHistocompatibility Antigens Class IIMiceMice, KnockoutUbiquitinationUbiquitin-Protein LigasesHistocompatibility Antigens Class IHistocompatibility Antigens Class IIMARCH1 protein, mouseUbiquitin-Protein Ligases

Identifiers

PMID30001419
PMCPMC6042767
OpenAlexW2813055229

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.