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

FGFR1 signaling in hypertrophic chondrocytes is attenuated by the Ras-GAP neurofibromin during endochondral bone formation.

Human molecular genetics - 1 May 2015

Karolak Matthew R, Yang Xiangli, Elefteriou Florent

Abstract excerpt

Aberrant fibroblast growth factor receptor 3 (FGFR3) signaling disrupts chondrocyte proliferation and growth plate size and architecture, leading to various chondrodysplasias or bone overgrowth. These observations suggest that the duration, intensity and cellular context of FGFR signaling during...

Read the complete abstract on PubMed

Topics

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

Share to Chondrogenesis
Share to Collagen Type II
Share to Growth Plate

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hypertrophy

Share to Neurofibromin 1

Share to Phenylurea Compounds

Share to Receptor, Fibroblast Growth Factor, Type 1

Share to Receptor, Fibroblast Growth Factor, Type 3

Source

Open in PubMed Open full text

Identifiers

PMID: 25616962
DOI: 10.1093/hmg/ddv019
PMCID: PMC4383864

Genes

FGFR1
FGFR3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-25616962-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

FGFR1 signaling in hypertrophic chondrocytes is attenuated by the Ras-GAP neurofibromin during endochondral bone formation.PMID 25616962Read ↗

Hyperactive Ras/MAPK signaling is critical for tibial nonunion fracture in neurofibromin-deficient miceSemantic proximity Read ↗

NF1 Tumor Suppressor Protein and mRNA in Skeletal Tissues of Developing and Adult Normal Mouse and NF1-Deficient EmbryosSemantic proximity Read ↗

Combined MEK Inhibition and BMP2 Treatment Promotes Osteoblast Differentiation and Bone Healing in Nf1Osx−/− MiceSemantic proximity Read ↗

Neurofibromin and its inactivation of Ras are prerequisites for osteoblast functioning.Semantic proximity Read ↗

Mice lacking Nf1 in osteochondroprogenitor cells display skeletal dysplasia similar to patients with neurofibromatosis type I.Semantic proximity Read ↗

Recent research on the growth plate: Advances in fibroblast growth factor signaling in growth plate development and disorders.Semantic proximity Read ↗

Constitutive activation of MEK1 in chondrocytes causes Stat1-independent achondroplasia-like dwarfism and rescues the Fgfr3-deficient mouse phenotype.Semantic proximity Read ↗

Coordination of chondrogenesis and osteogenesis by fibroblast growth factor 18.Semantic proximity Read ↗

An activating Fgfr3 mutation affects trabecular bone formation via a paracrine mechanism during growth.Semantic proximity Read ↗

Fibroblast growth factor receptor 3 is a negative regulator of bone growth.Semantic proximity Read ↗

Retinoid signaling regulates CTGF expression in hypertrophic chondrocytes with differential involvement of MAP kinases.Semantic proximity Read ↗

Runx2 Regulates Endochondral Ossification Through Control of Chondrocyte Proliferation and DifferentiationSemantic proximity Read ↗

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