Evidence map›Paper›PMID 30576947›Full record

ArticleMolecular immunology2019

Chemerin-activated functions of CMKLR1 are regulated by G protein-coupled receptor kinase 6 (GRK6) and β-arrestin 2 in inflammatory macrophages.

D Stephen Serafin, Brittney Allyn, Maria F Sassano, Roman G Timoshchenko, Daniel Mattox, Jaime M Brozowski, David P Siderovski, Young K Truong, Denise Esserman, Teresa K Tarrant and 1 more

Open access · greenAbstract read
In one paragraph

Article in Molecular immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Macrophage-Fibroblast Crosstalk Shapes Wound Repair Signaling In Vitro.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
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

11 authors at 3 institutions in 1 country.

D Stephen SerafinThurston Arthritis Research Center and the Department of Medicine, Division of Rheumatology, Allergy, and Immunology, University of North Carolina, Chapel Hill, NC 27599, United States.
Brittney AllynThurston Arthritis Research Center and the Department of Medicine, Division of Rheumatology, Allergy, and Immunology, University of North Carolina, Chapel Hill, NC 27599, United States; Duke University, Department of Medicine, Division of Rheumatology and Immunology, Durham, NC 27710, United States.
Maria F SassanoDepartment of Pharmacology, University of North Carolina, Chapel Hill, NC 27599, United States.
Roman G TimoshchenkoThurston Arthritis Research Center and the Department of Medicine, Division of Rheumatology, Allergy, and Immunology, University of North Carolina, Chapel Hill, NC 27599, United States.
Daniel MattoxThurston Arthritis Research Center and the Department of Medicine, Division of Rheumatology, Allergy, and Immunology, University of North Carolina, Chapel Hill, NC 27599, United States.
Jaime M BrozowskiDepartment of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC 27599, United States; Duke University, Department of Medicine, Division of Rheumatology and Immunology, Durham, NC 27710, United States.
David P SiderovskiDepartment of Physiology & Pharmacology, West Virginia University, Morgantown, WV, 26506, United States.
Young K TruongDepartment of Biostatistics, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC 27599, United States.
Denise EssermanYale School of Public Health, New Haven, CT 06510, United States.
Teresa K TarrantThurston Arthritis Research Center and the Department of Medicine, Division of Rheumatology, Allergy, and Immunology, University of North Carolina, Chapel Hill, NC 27599, United States; Duke University, Department of Medicine, Division of Rheumatology and Immunology, Durham, NC 27710, United States.
Matthew J BillardThurston Arthritis Research Center and the Department of Medicine, Division of Rheumatology, Allergy, and Immunology, University of North Carolina, Chapel Hill, NC 27599, United States; Department of Cell Biology and Physiology, University of North Carolina, Chapel Hill, NC 27599, United States. Electronic address: mbillard@unc.edu.
University of North Carolina at Chapel Hill · USWest Virginia University · USYale University · US

Funding

West Virginia IDEA-CTRU54GM104942 · NIGMS · WEST VIRGINIA UNIVERSITY · PI Reagan Curtis · 2012 to 2026
$81.0M
Modeling Lymphocyte Chemokine Receptor Dynamics and Polarization SignalsK01AI091863 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BILLARD, MATTHEW JOHN · 2012 to 2016
$423k
G protein-coupled receptor kinase 3 regulation of leukocyte function in inflammatR03AR059286 · NIAMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI TARRANT, TERESA KATHLEEN · 2011 to 2013
$218k
NIAID NIH HHS K01 AI091863NIAMS NIH HHS R03 AR059286NIGMS NIH HHS U54 GM104942
6 · The paper itself

Abstract

Chemerin receptor (CMKLR1) is a G protein-coupled receptor (GPCR) implicated in macrophage-mediated inflammation and in several forms of human arthritis. Analogous to other GPCR, CMKLR1 is likely regulated by G protein-coupled receptor kinase (GRK) phosphorylation of intracellular domains in an activation-dependent manner, which leads to recruitment and termination of intracellular signaling via desensitization and internalization of the receptor. The ubiquitously expressed GRK family members include GRK2, GRK3, GRK5, and GRK6, but it is unknown which GRK regulates CMKLR1 cellular and signaling functions. Our data show that activation of CMKLR1 by chemerin in primary macrophages leads to signaling and functional outcomes that are regulated by GRK6 and β-arrestin 2. We show that arrestin recruitment to CMKLR1 following chemerin stimulation is enhanced with co-expression of GRK6. Further, internalization of endogenous CMKLR1, following the addition of chemerin, is decreased in inflammatory macrophages from GRK6- and β-arrestin 2-deficient mice. These GRK6- and β-arrestin 2-deficient macrophages display increased migration toward chemerin and altered AKT and Extracellular-signal Related Kinase (ERK) signaling. Our findings show that chemerin-activated CMKLR1 regulation in inflammatory macrophages is largely GRK6 and β-arrestin mediated, which may impact innate immunity and have therapeutic implications in rheumatic disease.

Indexed as

Immunity, InnateAnimalsbeta-Arrestin 2Cell LineChemokinesG-Protein-Coupled Receptor KinasesHumansInflammationIntercellular Signaling Peptides and ProteinsMacrophagesMiceMice, KnockoutReceptors, ChemokineReceptors, G-Protein-CoupledRheumatic DiseasesArrb2 protein, mousebeta-Arrestin 2chemerin protein, mouseChemokinesCMKLR1 protein, mouseG-protein-coupled receptor kinase 6G-Protein-Coupled Receptor KinasesIntercellular Signaling Peptides and ProteinsReceptors, ChemokineReceptors, G-Protein-CoupledArrestinArthritisChemerinG protein-coupled receptor (GPCR)G protein-coupled receptor kinase (GRK)Macrophage

Identifiers

PMID30576947
PMCPMC6584946
OpenAlexW2904338307

What OpenQuestion holds

Textmetadata
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.