Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

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

Proceedings of the National Academy of Sciences of the United States of America - 26 Dec 2012

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

Abstract excerpt

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...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Bone and Bones
Share to Bone Development

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to GTP-Binding Protein alpha Subunits, Gi-Go

Share to Lumbar Vertebrae

Share to Mammals

Share to Mice, 129 Strain

Share to Mice, Mutant Strains

Source

Open in PubMed Open full text

Identifiers

PMID: 23236180
DOI: 10.1073/pnas.1219810110
PMCID: PMC3535641

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Development of the mammalian axial skeleton requires signaling through the Gα(i) subfamily of heterotrimeric G proteins.PMID 23236180Read ↗

Gnas Loss Causes Chondrocyte Fate Conversion in Cranial Suture FormationSemantic proximity Read ↗

Tgif1 and Tgif2 Regulate Axial Patterning in Mouse.Semantic proximity Read ↗

Chondrocyte-specific knockout of the G protein G(s)alpha leads to epiphyseal and growth plate abnormalities and ectopic chondrocyte formation.Semantic proximity Read ↗

Characterization of the skeletal fusion with sterility (sks) mouse showing axial skeleton abnormalities caused by defects of embryonic skeletal development.Semantic proximity Read ↗

Heterozygous inactivation of <i>Gnas</i> in adipose-derived mesenchymal progenitor cells enhances osteoblast differentiation and promotes heterotopic ossificationSemantic proximity Read ↗

Skeletal muscle deformity and neuronal disorder in Trio exchange factor-deficient mouse embryos.Semantic proximity Read ↗

The mouse rib-vertebrae mutation disrupts anterior-posterior somite patterning and genetically interacts with a Delta1 null allele.Semantic proximity Read ↗

G-Protein α-Subunit Gsα Is Required for Craniofacial Morphogenesis.Semantic proximity Read ↗

Multiple joint and skeletal patterning defects caused by single and double mutations in the mouse Gdf6 and Gdf5 genes.Semantic proximity Read ↗

Induced GnasR201H expression from the endogenous Gnas locus causes fibrous dysplasia by up-regulating Wnt/β-catenin signaling.Semantic proximity Read ↗

Wnt/β-catenin signaling is differentially regulated by Gα proteins and contributes to fibrous dysplasia.Semantic proximity Read ↗

Thoracic skeletal defects in myogenin- and MRF4-deficient mice correlate with early defects in myotome and intercostal musculature.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.