Evidence map›Paper›PMID 23236180›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Development of the mammalian axial skeleton requires signaling through the Gα(i) subfamily of heterotrimeric G proteins.

Nicholas W Plummer, Karsten Spicher, Jason Malphurs, Haruhiko Akiyama, Joel Abramowitz, Bernd Nürnberg, Lutz Birnbaumer

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. 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
1.5field-weighted citation impact, top 19% 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, 43 citations in OpenAlex.

  1. Review
  2. Gαi1/3 Is a Novel Regulatory Target for RANKL Signal Transduction and Osteoporosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Article
  4. Article
  5. GαInternational journal of molecular sciences · 2025
    Article
  6. Article
  7. Article
  8. Protective effects of GαNaunyn-Schmiedeberg's archives of pharmacology · 2024
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Lack of GαMolecular metabolism · 2020
    Article
  14. Selective protection of murine cerebral GJournal of molecular medicine (Berlin, Germany) · 2020
    Article
  15. Article
  16. Article
  17. GαJournal of immunology (Baltimore, Md. : 1950) · 2019
    Article
  18. GαOncotarget · 2018
    Article
  19. Review
  20. Gαi Proteins are Indispensable for Hearing.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018
    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

7 authors at 5 institutions in 3 countries.

Nicholas W PlummerLaboratory of Neurobiology, National Institute of Environmental Health Sciences, National Institutes of Health/Department of Health and Human Services, Durham, NC 27709, USA. plummer@niehs.nih.gov
Karsten Spicher
Jason Malphurs
Haruhiko Akiyama
Joel Abramowitz
Bernd Nürnberg
Lutz Birnbaumer
National Institutes of Health · USFederal Institute for Drugs and Medical Devices · DEKyoto University · JPNational Institute of Environmental Health Sciences · USUniversity of Tübingen · DE

Funding

Transmembrane Signaling MechanismsZIAES101643 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BIRNBAUMER, LUTZ · 2011 to 2014
$5.4M
Transmembrane Signaling MechanismsZ01ES101643 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BIRNBAUMER, LUTZ · 2003 to 2008
$5.1M
Intramural NIH HHS Z01 ES101643NIEHS NIH HHS Z01-ES-101643
6 · The paper itself

Abstract

129/SvEv mice with a loss-of-function mutation in the heterotrimeric G protein α-subunit gene Gnai3 have fusions of ribs and lumbar vertebrae, indicating a requirement for Gα(i) (the "inhibitory" class of α-subunits) in somite derivatives. Mice with mutations of Gnai1 or Gnai2 have neither defect, but loss of both Gnai3 and one of the other two genes increases the number and severity of rib fusions without affecting the lumbar fusions. No myotome defects are observed in Gnai3/Gnai1 double-mutant embryos, and crosses with a conditional allele of Gnai2 indicate that Gα(i) is specifically required in cartilage precursors. Penetrance and expressivity of the rib fusion phenotype is altered in mice with a mixed C57BL/6 × 129/SvEv genetic background. These phenotypes reveal a previously unknown role for G protein-coupled signaling pathways in development of the axial skeleton.

Indexed as

Bone DevelopmentSignal TransductionAllelesAnimalsBone and BonesGTP-Binding Protein alpha Subunit, Gi2GTP-Binding Protein alpha Subunits, Gi-GoLumbar VertebraeMammalsMiceMice, 129 StrainMice, Mutant StrainsMutationPhenotypeRibsSpinal FusionGnai2 protein, mouseGnai3 protein, mouseGTP-Binding Protein alpha Subunit, Gi2GTP-Binding Protein alpha Subunits, Gi-Go

Identifiers

PMID23236180
PMCPMC3535641
OpenAlexW1967211967

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.