Evidence map›Paper›PMID 24727021›Full record

ArticleGastroenterology2014

Copper metabolism domain-containing 1 represses genes that promote inflammation and protects mice from colitis and colitis-associated cancer.

Haiying Li, Lillienne Chan, Paulina Bartuzi, Shelby D Melton, Axel Weber, Shani Ben-Shlomo, Chen Varol, Megan Raetz, Xicheng Mao, Petro Starokadomskyy and 19 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.8field-weighted citation impact, top 11% 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

33 citing papers in PubMed, 46 citations in OpenAlex.

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  14. Structural Organization of the Retriever-CCC Endosomal Recycling Complex.bioRxiv : the preprint server for biology · 2023
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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

29 authors at 9 institutions in 5 countries.

Haiying LiDepartment of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
Lillienne ChanDepartment of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
Paulina BartuziDepartment of Pediatrics (Section of Molecular Genetics), University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Shelby D MeltonDepartment of Pathology, Dallas VA Medical Center, Dallas, Texas.
Axel WeberRudolf Buchheim Institute of Pharmacology, Justus Liebig University, Giessen, Germany.
Shani Ben-ShlomoGastroenterology Institute, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel.
Chen VarolGastroenterology Institute, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel.
Megan RaetzDepartment of Immunology, University of Texas Southwestern Medical Center, Dallas, Texas.
Xicheng MaoDepartment of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
Petro StarokadomskyyDepartment of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
Suzanne van SommerenDepartment of Gastroenterology and Hepatology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Mohamad MokademDepartment of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
Heike SchneiderInstitute of Physiological Chemistry, Hannover Medical School, Hannover, Germany.
Reid WeisbergDepartment of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
Harm-Jan WestraDepartment of Genetics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Tõnu EskoEstonian Genome Center, University of Tartu, Tartu, Estonia.
Andres MetspaluEstonian Genome Center, University of Tartu, Tartu, Estonia.
Vinod KumarDepartment of Genetics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
William A FaubionDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota.
Felix YarovinskyDepartment of Immunology, University of Texas Southwestern Medical Center, Dallas, Texas.
Marten HofkerDepartment of Pediatrics (Section of Molecular Genetics), University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Cisca WijmengaDepartment of Genetics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Michael KrachtRudolf Buchheim Institute of Pharmacology, Justus Liebig University, Giessen, Germany.
Lude FrankeDepartment of Genetics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Vincent AguirreDepartment of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
Rinse K WeersmaDepartment of Gastroenterology and Hepatology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Nathan GluckGastroenterology Institute, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel.
Bart van de SluisDepartment of Pediatrics (Section of Molecular Genetics), University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Ezra BursteinDepartment of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas. Electronic address: ezra.burstein@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · USUniversity Medical Center Groningen · NLTel Aviv Sourasky Medical Center · ILUniversity of Groningen · NLUniversity of Giessen · DEUniversity of Tartu · EEDallas VA Medical Center · USMayo Clinic · USMedizinische Hochschule Hannover · DE

Funding

UT GASTROENTEROLOGY/HEPATOLOGY RESEARCH TRAINING PROGRAMT32DK007745 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI Rodney E Infante · 1997 to 2026
$6.8M
Role of the CCC complex in immune functionR01DK073639 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI BURSTEIN, EZRA · 2007 to 2020
$3.7M
NIDDK NIH HHS R01 DK073639NIDDK NIH HHS T32 DK007745
6 · The paper itself

Abstract

BACKGROUND &

aimsActivation of the transcription factor nuclear factor-κB (NF-κB) has been associated with the development of inflammatory bowel disease (IBD). Copper metabolism MURR1 domain containing 1 (COMMD1), a regulator of various transport pathways, has been shown to limit NF-κB activation. We investigated the roles of COMMD1 in the pathogenesis of colitis in mice and IBD in human beings.

methodsWe created mice with a specific disruption of Commd1 in myeloid cells (Mye-knockout [K/O] mice); we analyzed immune cell populations and functions and expression of genes regulated by NF-κB. Sepsis was induced in Mye-K/O and wild-type mice by cecal ligation and puncture or intraperitoneal injection of lipopolysaccharide (LPS), colitis was induced by administration of dextran sodium sulfate, and colitis-associated cancer was induced by administration of dextran sodium sulfate and azoxymethane. We measured levels of COMMD1 messenger RNA in colon biopsy specimens from 29 patients with IBD and 16 patients without (controls), and validated findings in an independent cohort (17 patients with IBD and 22 controls). We searched for polymorphisms in or near COMMD1 that were associated with IBD using data from the International IBD Genetics Consortium and performed quantitative trait locus analysis.

resultsIn comparing gene expression patterns between myeloid cells from Mye-K/O and wild-type mice, we found that COMMD1 represses expression of genes induced by LPS. Mye-K/O mice had more intense inflammatory responses to LPS and developed more severe sepsis and colitis, with greater mortality. More Mye-K/O mice with colitis developed colon dysplasia and tumors than wild-type mice. We observed a reduced expression of COMMD1 in colon biopsy specimens and circulating leukocytes from patients with IBD. We associated single-nucleotide variants near COMMD1 with reduced expression of the gene and linked them with increased risk for ulcerative colitis.

conclusionsExpression of COMMD1 by myeloid cells has anti-inflammatory effects. Reduced expression or function of COMMD1 could be involved in the pathogenesis of IBD.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAzoxymethaneBiopsyCase-Control StudiesColitisColonColonic NeoplasmsDextran SulfateDisease Models, AnimalHumansInflammationInflammatory Bowel DiseasesMiceMice, KnockoutNF-kappa BAdaptor Proteins, Signal TransducingAzoxymethaneCOMMD1 protein, humanCommd1 protein, mouseDextran SulfateNF-kappa BRNA, MessengerCDGene RegulationMouse ModelUC

Identifiers

PMID24727021
PMCPMC4086320
OpenAlexW1968959442

What OpenQuestion holds

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LicenceTDM
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.