Evidence map›Paper›PMID 30356278›Full record

ArticlePloS one2018

The E3 ubiquitin ligase MARCH1 regulates glucose-tolerance and lipid storage in a sex-specific manner.

Candida Bhagwandin, Erin L Ashbeck, Michael Whalen, Joanna Bandola-Simon, Paul A Roche, Adam Szajman, Sarah Mai Truong, Betsy C Wertheim, Yann C Klimentidis, Satoshi Ishido and 2 more

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 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
0.6field-weighted citation impact, top 28% 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, 23 citations in OpenAlex.

  1. Pooled it
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  5. E3 ubiquitin ligase MARCH1 reduces inflammation and pyroptosis in cerebral ischemia-reperfusion injury via PCSK9 downregulation.Mammalian genome : official journal of the International Mammalian Genome Society · 2024
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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

12 authors at 3 institutions in 2 countries.

Candida BhagwandinCellular and Molecular Medicine, University of Arizona, Tucson, Arizona, United States of America.
Erin L AshbeckUniversity of Arizona Cancer Center, University of Arizona, Tucson, Arizona, United States of America.
Michael WhalenCellular and Molecular Medicine, University of Arizona, Tucson, Arizona, United States of America.
Joanna Bandola-SimonExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, United States of America.
Paul A RocheExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, United States of America.
Adam SzajmanMolecular and Cellular Biology, University of Arizona, Tucson, Arizona, United States of America.
Sarah Mai TruongMolecular and Cellular Biology, University of Arizona, Tucson, Arizona, United States of America.
Betsy C WertheimUniversity of Arizona Cancer Center, University of Arizona, Tucson, Arizona, United States of America.
Yann C KlimentidisMel and Enid Zuckerman College of Public Health, Department of Epidemiology and Biostatistics, University of Arizona, Tucson, Arizona, United States of America.
Satoshi IshidoDepartment of Microbiology, Hyogo College of Medicine, Nishinomiya, Japan.
Benjamin J RenquistAnimal and Comparative Biomedical Sciences, University of Arizona, Tucson, Arizona, United States of America.
Lonnie LybargerCellular and Molecular Medicine, University of Arizona, Tucson, Arizona, United States of America.ORCID 0000-0001-5703-3792
University of Arizona · USNational Institutes of Health · USHyogo Medical University · JP

Funding

Statistical MethodsP01CA087969 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI TWOROGER, SHELLEY S · 2000 to 2019
$77.8M
VANDERBILT UNIVERSITY CTSA FOR PEDIATRIC RESEARCHUL1RR024975 · NCRR · VANDERBILT UNIVERSITY · PI BERNARD, GORDON RAPHAEL · 2007 to 2011
$45.7M
Validity of Diet and Activity Measures in WomenP01CA055075 · NCI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI WILLETT, WALTER C. · 1991 to 2009
$41.8M
A Center for GEI Association StudiesU01HG004424 · NHGRI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI GABRIEL, STACEY · 2007 to 2010
$21.4M
Regulation of MHC Class II Trafficking in Antigen Presenting CellsZIABC009404 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI ROCHE, PAUL · 2009 to 2025
$17.9M
BIOCHEMICAL AND GENETIC MARKERS OF TYPE 2 DIABETES RISKR01DK058845 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI HU, FRANK B · 2001 to 2013
$7.8M
Vanderbilt Genome-Electronic Records ProjectU01HG004603 · NHGRI · VANDERBILT UNIVERSITY · PI RODEN, DAN M · 2007 to 2011
$7.3M
Genome Wide Association Coordinating CenterU01HG004446 · NHGRI · UNIVERSITY OF WASHINGTON · PI WEIR, BRUCE S. · 2007 to 2011
$6.6M
Genome-wide Studies from the NUgene BiorespositoryU01HG004609 · NHGRI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CHISHOLM, REX L · 2007 to 2010
$3.7M
Genes and Environment Initiatives in Type 2 DiabetesU01HG004399 · NHGRI · HARVARD SCHOOL OF PUBLIC HEALTH · PI HU, FRANK B · 2007 to 2008
$1.2M
UBIQUITIN-DEPENDENT REGULATION OF IMMUNE ACTIVATIONR56AI080756 · NIAID · UNIVERSITY OF ARIZONA · PI LYBARGER, LONNIE P · 2010 to 2010
$335k
NCI NIH HHS P01 CA055075NCI NIH HHS P01 CA087969NCRR NIH HHS UL1 RR024975NHGRI NIH HHS U01 HG004399NHGRI NIH HHS U01 HG004424NHGRI NIH HHS U01 HG004446NHGRI NIH HHS U01 HG004603NHGRI NIH HHS U01 HG004609NIAID NIH HHS R56 AI080756NIDDK NIH HHS R01 DK058845
6 · The paper itself

Abstract

Type 2 diabetes is typified by insulin-resistance in adipose tissue, skeletal muscle, and liver, leading to chronic hyperglycemia. Additionally, obesity and type 2 diabetes are characterized by chronic low-grade inflammation. Membrane-associated RING-CH-1 (MARCH1) is an E3 ubiquitin ligase best known for suppression of antigen presentation by dendritic and B cells. MARCH1 was recently found to negatively regulate the cell surface levels of the insulin receptor via ubiquitination. This, in turn, impaired insulin sensitivity in mouse models. Here, we report that MARCH1-deficient (knockout; KO) female mice exhibit excessive weight gain and excessive visceral adiposity when reared on standard chow diet, without increased inflammatory cell infiltration of adipose tissue. By contrast, male MARCH1 KO mice had similar weight gain and visceral adiposity to wildtype (WT) male mice. MARCH1 KO mice of both sexes were more glucose tolerant than WT mice. The levels of insulin receptor were generally higher in insulin-responsive tissues (especially the liver) from female MARCH1 KO mice compared to males, with the potential to account in part for the differences between male and female MARCH1 KO mice. We also explored a potential role for MARCH1 in human type 2 diabetes risk through genetic association testing in publicly-available datasets, and found evidence suggestive of association. Collectively, our data indicate an additional link between immune function and diabetes, specifically implicating MARCH1 as a regulator of lipid metabolism and glucose tolerance, whose function is modified by sex-specific factors.

Indexed as

AdiposityAnimalsCase-Control StudiesDatabases, GeneticDiabetes Mellitus, Type 2FemaleGene Knockout TechniquesGenetic Association StudiesGlucose Tolerance TestHumansMaleMicePolymorphism, Single NucleotideSex FactorsUbiquitin-Protein LigasesWeight GainMARCH1 protein, mouseMARCHF1 protein, humanUbiquitin-Protein Ligases

Identifiers

PMID30356278
PMCPMC6200199
OpenAlexW2898589255

What OpenQuestion holds

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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.