ArticleCell discovery2017
RNA-binding protein SAMD4 regulates skeleton development through translational inhibition of Mig6 expression.
Article in Cell discovery, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- Chiral FeBioactive materials · 2026Article
- Article
- Single-cell RNA sequencing of healthy and diseased rat temporomandibular joint condyle cartilage.PloS one · 2026Article
- SAMD4A inhibits abdominal aortic aneurysm development and VSMC phenotypic transformation through targeting KDM2B.Journal of advanced research · 2026Article
- Oncogenic Role of SAMD4B in Breast Cancer Progression by Activating Wnt/β-Catenin Pathway.Biomolecules · 2025Article
- Article
- RNA-binding protein SAMD4A targets FGF2 to regulate cardiomyocyte lineage specification from human embryonic stem cells.Stem cell research & therapy · 2025Article
- Dynamic mRNA Stability Buffer Transcriptional Activation During Neuronal Differentiation and Is Regulated by SAMD4A.Journal of cellular physiology · 2025Article
- RNA-binding proteins regulate osteoarthritis via RNA metabolism regulation.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Review
- Recent Progress in the Research on RNA-Binding Proteins in Bone Development and Diseases.International journal of molecular sciences · 2024Review
- RNA-binding proteins in bone pathophysiology.Frontiers in cell and developmental biology · 2024Review
- Structural basis for binding ofProceedings of the National Academy of Sciences of the United States of America · 2023Article
- RNA binding protein SAMD4: current knowledge and future perspectives.Cell & bioscience · 2023Review
- Article
- RNA-binding proteins that are highly expressed and enriched in healthy cartilage but suppressed in osteoarthritis.Frontiers in cell and developmental biology · 2023Article
- In heart failure reactivation of RNA-binding proteins is associated with the expression of 1,523 fetal-specific isoforms.PLoS computational biology · 2022Article
- A novel testis-enriched gene,Frontiers in cell and developmental biology · 2022Article
- RNA binding proteins in osteoarthritis.Frontiers in cell and developmental biology · 2022Review
- Expression and Regulatory Network Analysis of BICC1 for Aged Sca-1-Positive Bone Narrow Mesenchymal Stem Cells.Disease markers · 2022Article
- SAMD4 family members suppress human hepatitis B virus by directly binding to the Smaug recognition region of viral RNA.Cellular & molecular immunology · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein translation regulation has essential roles in inflammatory responses, cancer initiation and the pathogenesis of several neurodegenerative disorders. However, the role of the regulation of protein translation in mammalian skeleton development has been rarely elaborated. Here we report that the lack of the RNA-binding protein sterile alpha motif domain containing protein 4 (SAMD4) resulted in multiple developmental defects in mice, including delayed bone development and decreased osteogenesis. Samd4-deficient mesenchymal progenitors exhibit impaired osteoblast differentiation and function. Mechanism study demonstrates that SAMD4 binds the Mig6 mRNA and inhibits MIG6 protein synthesis. Consistent with this, Samd4-deficient cells have increased MIG6 protein level and knockdown of Mig6 rescues the impaired osteogenesis in Samd4-deficient cells. Furthermore, Samd4-deficient mice also display chondrocyte defects, which is consistent with the regulation of MIG6 protein level by SAMD4. These findings define SAMD4 as a previously unreported key regulator of osteoblastogenesis and bone development, implying that regulation of protein translation is an important mechanism governing skeletogenesis and that control of protein translation could have therapeutic potential in metabolic bone diseases, such as osteoporosis.
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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.