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

Transcriptomic Signature and Pro-Osteoclastic Secreted Factors of Abnormal Bone-Marrow Stromal Cells in Fibrous Dysplasia

30 Apr 2024

Abstract excerpt

Fibrous dysplasia (FD) is a mosaic skeletal disorder caused by somatic activating variants of GNAS encoding for Gαs and leading to excessive cyclic adenosine monophosphate signaling in bone-marrow stromal cells (BMSCs). The effect of Gαs activation in the BMSC transcriptome and how it influences FD lesion microenvironment are unclear. We analyzed changes induced by Gαs activation in the BMSC transcriptome and...

Read the complete abstract on PubMed

Topics

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

Share to Bone health and treatments
Share to Bone Tumor Diagnosis and Treatments
Share to Oral and Maxillofacial Pathology

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 38727310
DOI: 10.3390/cells13090774

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Transcriptomic Signature and Pro-Osteoclastic Secreted Factors of Abnormal Bone-Marrow Stromal Cells in Fibrous DysplasiaPMID 38727310Read ↗

Transcriptomic signature and pro-osteoclastic secreted factors of abnormal bone marrow stromal cells in fibrous dysplasiaSemantic proximity Read ↗

Single-cell analysis of human fibrous dysplasia bone reveals a fibrotic transcriptome and GNAS variants in endothelial, perivascular, and stromal cellsSemantic proximity Read ↗

The CREB–Smad6–Runx2 axis contributes to the impaired osteogenesis potential of bone marrow stromal cells in fibrous dysplasia of boneSemantic proximity Read ↗

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

Skeletal progenitors and the GNAS gene: fibrous dysplasia of bone read through stem cells.Semantic proximity Read ↗

A Signature of Circulating miRNAs Associated With Fibrous Dysplasia of Bone: the mirDys StudySemantic proximity Read ↗

Fibrous dysplasia/McCune-Albright syndrome: state-of-the-art advances, pathogenesis, and basic/translational researchSemantic proximity Read ↗

RANKL inhibition reduces lesional cellularity and Gαs variant expression and enables osteogenic maturation in fibrous dysplasiaSemantic proximity Read ↗

RANKL inhibition reduces lesional cellularity, Gαs variant expression and enables osteogenic maturation in fibrous dysplasiaSemantic proximity Read ↗

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

Osteoblast-Specific Expression of the Fibrous Dysplasia (FD)–Causing Mutation <i>GsαR201C</i> Produces a High Bone Mass Phenotype but Does Not Reproduce FD in the MouseSemantic proximity Read ↗

Fibrous Dysplasia/McCune-Albright Syndrome: A Rare, Mosaic Disease of Gα s ActivationSemantic proximity Read ↗

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