Evidence map›Paper›PMID 33469151›Full record

ArticleCommunications biology2021

LRIG proteins regulate lipid metabolism via BMP signaling and affect the risk of type 2 diabetes.

Carl Herdenberg, Pascal M Mutie, Ola Billing, Ahmad Abdullah, Rona J Strawbridge, Ingrid Dahlman, Simon Tuck, Camilla Holmlund, Peter Arner, Roger Henriksson and 2 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.5field-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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

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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.

Carl HerdenbergDepartment of Radiation Sciences, Oncology, Umeå University, SE-90187, Umeå, Sweden.
Pascal M MutieGenetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Lund University, Skane University Hospital, Malmo, Sweden.
Ola BillingDepartment of Surgical and Perioperative Sciences, Surgery, Umeå University, SE-90187, Umeå, Sweden.ORCID 0000-0001-5824-6263
Ahmad AbdullahDepartment of Radiation Sciences, Oncology, Umeå University, SE-90187, Umeå, Sweden.ORCID 0000-0003-3502-5948
Rona J StrawbridgeInstitute of Health and Wellbeing, University of Glasgow, Glasgow, UK.ORCID 0000-0001-8506-3585
Ingrid DahlmanDepartment of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden.
Simon TuckUmeå Center for Molecular Medicine, Umeå University, SE-90187, Umeå, Sweden.
Camilla HolmlundDepartment of Radiation Sciences, Oncology, Umeå University, SE-90187, Umeå, Sweden.
Peter ArnerDepartment of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-6208-6220
Roger HenrikssonDepartment of Radiation Sciences, Oncology, Umeå University, SE-90187, Umeå, Sweden.
Paul W FranksGenetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Lund University, Skane University Hospital, Malmo, Sweden.ORCID 0000-0002-0520-7604
Håkan HedmanDepartment of Radiation Sciences, Oncology, Umeå University, SE-90187, Umeå, Sweden. hakan.hedman@umu.se.ORCID 0000-0001-6891-6996
Umeå University · SEKarolinska Institutet · SELund University · SE

Funding

Medical Research Council MR/S003061/1
6 · The paper itself

Abstract

Leucine-rich repeats and immunoglobulin-like domains (LRIG) proteins have been implicated as regulators of growth factor signaling; however, the possible redundancy among mammalian LRIG1, LRIG2, and LRIG3 has hindered detailed elucidation of their physiological functions. Here, we show that Lrig-null mouse embryonic fibroblasts (MEFs) are deficient in adipogenesis and bone morphogenetic protein (BMP) signaling. In contrast, transforming growth factor-beta (TGF-β) and receptor tyrosine kinase (RTK) signaling appeared unaltered in Lrig-null cells. The BMP signaling defect was rescued by ectopic expression of LRIG1 or LRIG3 but not by expression of LRIG2. Caenorhabditis elegans with mutant LRIG/sma-10 variants also exhibited a lipid storage defect. Human LRIG1 variants were strongly associated with increased body mass index (BMI) yet protected against type 2 diabetes; these effects were likely mediated by altered adipocyte morphology. These results demonstrate that LRIG proteins function as evolutionarily conserved regulators of lipid metabolism and BMP signaling and have implications for human disease.

Indexed as

AdipogenesisAdultAgedAnimalsBody Mass IndexBone Morphogenetic ProteinsCaenorhabditis elegansDiabetes Mellitus, Type 2FemaleFibroblastsHumansLipid MetabolismMaleMembrane GlycoproteinsMembrane ProteinsMiceBone Morphogenetic ProteinsLRIG1 protein, humanLRIG3 protein, humanMembrane GlycoproteinsMembrane Proteins

Identifiers

PMID33469151
PMCPMC7815736
OpenAlexW3124685089

What OpenQuestion holds

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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.