ArticleNature communications2025
Nf2-FAK signaling axis is critical for cranial bone ossification and regeneration.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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.
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Who cites it
8 citing papers in PubMed.
- Lysine l-Lactylation: Bridging Metabolism, Chromatin and Disease.Cell proliferation · 2026Review
- Nf2 orchestrates β-arrestin2-biased PTH1R signaling to couple bone mass with skeletal integrity.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Strategy based on liquid crystal elastomer active tensile to accelerate bone repair: Mechanistic analysis of LAMB1-ITGB4 mediated PI3K-AKT signaling.Materials today. Bio · 2026Article
- Article
- Circulating Exosomal MicroRNA Profiles Associated with Heavy Metal Exposure and Short Stature in Children.International journal of molecular sciences · 2026Article
- TGF-β/BMP signaling in skeletal biology: molecular mechanisms, regulatory networks, and therapeutic implications in development, regeneration, and disease.Bone research · 2026Review
- Nf2/FGFR1/AKT axis directs cranial neural crest-derived skull morphogenesis via collagen synthesis and trafficking.JCI insight · 2025Article
- Hedgehog Signalling in Osteogenesis and Bone Metabolism: Molecular Mechanisms, Regulatory Networks and Implications for Skeletal Disease.Journal of cellular and molecular medicine · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Skeletal mesenchymal stem cells (MSCs) possess self-renewal capacities and play a leading role in the craniofacial system. However, their engagement in controlling cranial bone development and regeneration remains largely unidentified. Herein, we discovered the neurofibromin 2 (Nf2)-encoded regulator Merlin, demonstrating indispensableness in the craniofacial system. Mice lacking Nf2 in MSCs exhibit malformed cranial bones, diminished proliferation, increased apoptosis, and more severe osteogenesis impairment. Mechanically, we substantiate that Nf2 physically interacts with focal adhesion kinase (FAK) to preferentially mediate Erk1/2 and PI3K catalytic p110 subunit/Akt signaling. Meanwhile, Nf2-FAK disturbance in MSCs results in deficient migration, cytoskeletal organization and focal adhesion dynamics, and develops retarded regeneration of cranial bone defects. Collectively, our findings underscore an unrecognized scaffolding role for Nf2-FAK as upstream element in regulating PI3K/Akt and Erk1/2 action in osteoblasts, and illuminate its essentialness in coordinating cell migration, osteogenic lineage development, cranial bone ossification and regeneration.
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Registered trials
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.