Evidence map›Paper›PMID 29371232›Full record

ArticleThe Journal of cell biology2018

MARCH1 protects the lipid raft and tetraspanin web from MHCII proteotoxicity in dendritic cells.

Jaehak Oh, Justin S A Perry, Heather Pua, Nicole Irgens-Möller, Satoshi Ishido, Chyi-Song Hsieh, Jeoung-Sook Shin

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
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  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Ubiquitination of MHC Class II by March-I Regulates Dendritic Cell Fitness.Journal of immunology (Baltimore, Md. : 1950) · 2021
    Article
  9. Review
  10. Review
  11. Article
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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

7 authors at 3 institutions in 2 countries.

Jaehak OhDepartment of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA.ORCID 0000-0003-3079-5927
Justin S A PerryDepartment of Pathology, University of California, San Francisco, San Francisco, CA.
Heather PuaSandler Asthma Basic Research Center, University of California, San Francisco, San Francisco, CA.ORCID 0000-0002-9271-2608
Nicole Irgens-MöllerDepartment of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA.
Satoshi IshidoDepartment of Microbiology, Hyogo College of Medicine 1-1, Mukogawa-cho, Nishinomiya, Japan.
Chyi-Song HsiehDepartment of Internal Medicine, Division of Rheumatology, Washington University School of Medicine, St. Louis, MO.
Jeoung-Sook ShinDepartment of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA jeoung-sook.shin@ucsf.edu.ORCID 0000-0002-0711-8234
University of California, San Francisco · USHyogo Medical University · JPWashington University in St. Louis · US

Funding

UNIQUE ROLES OF ANTIGEN PRESENTING CELLS ON T CELL TOLERANCE AND AUTOIMMUNITYR01AI079187 · NIAID · WASHINGTON UNIVERSITY · PI HSIEH, CHYI S · 2008 to 2021
$5.8M
Role of MARCH1 E3 ubiquitin ligase in thymic dendritic cell functionR01GM105800 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SHIN, JEOUNG-SOOK · 2013 to 2017
$1.5M
NIAID NIH HHS R01 AI079187NIGMS NIH HHS R01 GM105800
6 · The paper itself

Abstract

Dendritic cells (DCs) produce major histocompatibility complex II (MHCII) in large amounts to function as professional antigen presenting cells. Paradoxically, DCs also ubiquitinate and degrade MHCII in a constitutive manner. Mice deficient in the MHCII-ubiquitinating enzyme membrane-anchored RING-CH1, or the ubiquitin-acceptor lysine of MHCII, exhibit a substantial reduction in the number of regulatory T (Treg) cells, but the underlying mechanism was unclear. Here we report that ubiquitin-dependent MHCII turnover is critical to maintain homeostasis of lipid rafts and the tetraspanin web in DCs. Lack of MHCII ubiquitination results in the accumulation of excessive quantities of MHCII in the plasma membrane, and the resulting disruption to lipid rafts and the tetraspanin web leads to significant impairment in the ability of DCs to engage and activate thymocytes for Treg cell differentiation. Thus, ubiquitin-dependent MHCII turnover represents a novel quality-control mechanism by which DCs maintain homeostasis of membrane domains that support DC's Treg cell-selecting function.

Indexed as

Cell CommunicationAdoptive TransferAnimalsCell DifferentiationCells, CulturedCoculture TechniquesDendritic CellsHistocompatibility Antigens Class IIHomeostasisLymphocyte ActivationMembrane MicrodomainsMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutPhenotypeReceptors, Antigen, T-CellHistocompatibility Antigens Class IIMARCH1 protein, mouseReceptors, Antigen, T-CellTetraspaninsUbiquitin-Protein Ligases

Identifiers

PMID29371232
PMCPMC5881489
OpenAlexW2785253162

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.