Evidence map›Paper›PMID 31173907›Full record

ArticleBone2019

A role for G protein-coupled receptor 137b in bone remodeling in mouse and zebrafish.

K Urso, J Caetano-Lopes, P Y Lee, J Yan, K Henke, M Sury, H Liu, M Zgoda, C Jacome-Galarza, P A Nigrovic and 3 more

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

Article in Bone, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Fish Models of Induced Osteoporosis.Frontiers in cell and developmental biology · 2021
    Review
  7. 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

13 authors at 3 institutions in 1 country.

K UrsoDepartment of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
J Caetano-LopesDepartment of Orthopedic Research, Boston Children's Hospital, Boston, MA, USA; Department of Genetics, Harvard Medical School, Boston, MA, USA.
P Y LeeDepartment of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA; Division of Immunology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
J YanDepartment of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
K HenkeDepartment of Orthopedic Research, Boston Children's Hospital, Boston, MA, USA; Department of Genetics, Harvard Medical School, Boston, MA, USA.
M SuryDepartment of Orthopedic Research, Boston Children's Hospital, Boston, MA, USA; Department of Genetics, Harvard Medical School, Boston, MA, USA; Department of Radiology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
H LiuDepartment of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
M ZgodaDepartment of Orthopedics, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
C Jacome-GalarzaDepartment of Orthopedics, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
P A NigrovicDepartment of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA; Division of Immunology, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA.
J DuryeaDepartment of Radiology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
M P HarrisDepartment of Orthopedic Research, Boston Children's Hospital, Boston, MA, USA; Department of Genetics, Harvard Medical School, Boston, MA, USA.
J F CharlesDepartment of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA; Department of Orthopedics, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. Electronic address: jfcharles@bwh.harvard.edu.
Brigham and Women's Hospital · USHarvard University · USBoston Children's Hospital · US

Funding

MOLECULAR BASIS OF ALLERGIC AND IMMUNOLOGIC DISEASET32AI007512 · NIAID · CHILDREN'S HOSPITAL BOSTON · PI Janet Chou, Peter A Nigrovic · 1996 to 2026
$13.1M
Joint Biology Consortium Resource-based CenterP30AR070253 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI Peter A Nigrovic, Jeffrey Andrew Sparks · 2016 to 2026
$9.4M
Ly6 family members in neutrophil biologyR01AR065538 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI NIGROVIC, PETER A · 2014 to 2024
$4.0M
Skeletal Phenotyping CoreP30AR066261 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI DIVIETI PAJEVIC, PAOLA · 2014 to 2018
$3.5M
Anatomical atlas and transgenic toolkit for late skull formation in zebrafishU01DE024434 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI FISHER, SHANNON, HARRIS, MATTHEW P · 2014 to 2018
$3.3M
Regulation of osteoclast biology by anion exchanger SLC4A2 in mouse and human sysR01AR060363 · NIAMS · HARVARD SCHOOL OF PUBLIC HEALTH · PI CHARLES, JULIA F · 2011 to 2015
$1.9M
Osteoclast precursors in bone homeostasis and inflammatory arthritisK08AR062590 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI CHARLES, JULIA F · 2012 to 2016
$619k
NIAID NIH HHS T32 AI007512NIAMS NIH HHS K08 AR062590NIAMS NIH HHS P30 AR066261NIAMS NIH HHS P30 AR070253NIAMS NIH HHS R01 AR060363NIAMS NIH HHS R01 AR065538NIDCR NIH HHS U01 DE024434
6 · The paper itself

Abstract

G protein-coupled receptor 137b (GPR137b) is an orphan seven-pass transmembrane receptor of unknown function. In mouse, Gpr137b is highly expressed in osteoclasts in vivo and is upregulated during in vitro differentiation. To elucidate the role that GPR137b plays in osteoclasts, we tested the effect of GPR137b deficiency on osteoclast maturation and resorbing activity. We used CRISPR/Cas9 gene editing in mouse-derived ER-Hoxb8 immortalized myeloid progenitors to generate GPR137b-deficient osteoclast precursors. Decreasing Gpr137b in these precursors led to increased osteoclast differentiation and bone resorption activity. To explore the role of GPR137b during skeletal development, we generated zebrafish deficient for the ortholog gpr137ba. Gpr137ba-deficient zebrafish are viable and fertile and do not display overt morphological defects as adults. However, analysis of osteoclast function in gpr137ba

Indexed as

AnimalsBase SequenceBone and BonesBone RemodelingBone ResorptionCell DifferentiationHomeostasisLoss of Function MutationMice, Inbred C57BLOsteoclastsOsteogenesisReceptors, G-Protein-CoupledZebrafishZebrafish Proteinsgpr137ba protein, zebrafishGpr137b protein, mouseReceptors, G-Protein-CoupledZebrafish ProteinsBoneGPR137bOsteoclastZebrafish

Identifiers

PMID31173907
PMCPMC6708790
OpenAlexW2948952822

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.