Evidence map›Paper›PMID 28049723›Full record

ArticleJournal of cell science2017

Defective signaling, osteoblastogenesis and bone remodeling in a mouse model of connexin 43 C-terminal truncation.

Megan C Moorer, Carla Hebert, Ryan E Tomlinson, Shama R Iyer, Max Chason, Joseph P Stains

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cell science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

49 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Injury-induced connexin 43 expression regulates endothelial wound healing.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  3. Osteocyte connexin hemichannels and prostaglandin EProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Independent contribution of gonads and sex chromosomes to sex differences in bone mass and strength in the four-core genotypes mouse model.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024
    Article
  5. Nitric oxide contributes to rapid sclerostin protein loss following mechanical load.Biochemical and biophysical research communications · 2024
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Connexin 43 hemichannels and prostaglandin EFrontiers in cell and developmental biology · 2023
    Review
  16. Article
  17. Review
  18. Article
  19. Similarities Between Disuse and Age-Induced Bone Loss.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
    Review
  20. Article
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

6 authors at 2 institutions in 1 country.

Megan C MoorerDepartment of Orthopaedics, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Carla HebertDepartment of Orthopaedics, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Ryan E TomlinsonDepartment of Orthopaedic Surgery, Johns Hopkins University, Baltimore, MD 21287, USA.
Shama R IyerDepartment of Orthopaedics, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Max ChasonDepartment of Orthopaedics, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Joseph P StainsDepartment of Orthopaedics, University of Maryland School of Medicine, Baltimore, MD 21201, USA jstains@som.umaryland.edu.ORCID 0000-0002-1610-4694
University of Maryland, Baltimore · USJohns Hopkins University · US

Funding

Spatial Control of Bone Remodeling by Gap Junction-Communicated cAMPR01AR063631 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI STAINS, JOSEPH P. · 2013 to 2024
$3.3M
Intercellular Signaling in BoneR01AR052719 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI STAINS, JOSEPH P. · 2006 to 2010
$1.3M
NIAMS NIH HHS R01 AR052719NIAMS NIH HHS R01 AR063631
6 · The paper itself

Abstract

In skeletal tissue, loss or mutation of the gap junction protein connexin 43 (Cx43, also known as GJA1) in cells of the osteoblast lineage leads to a profound cortical bone phenotype and defective tissue remodeling. There is mounting evidence in bone cells that the C-terminus (CT) of Cx43 is a docking platform for signaling effectors and is required for efficient downstream signaling. Here, we examined this function, using a mouse model of Cx43 CT-truncation (Gja1 K258Stop). Relative to Gja1

Indexed as

Bone RemodelingOsteogenesisSignal TransductionAnimalsBone ResorptionCalcification, PhysiologicCell DifferentiationCell ProliferationCollagenConnexin 43Cortical BoneExtracellular MatrixMaleMiceModels, AnimalOsteoblastsCollagenConnexin 43RNA, MessengerCx43 K258StopGap junctionIntercellular communicationOsteoblastOsteocyteSignal transduction

Identifiers

PMID28049723
PMCPMC5312734
OpenAlexW2562819638

What OpenQuestion holds

Textmetadata
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.