ArticleNature communications2021
SLITRK5 is a negative regulator of hedgehog signaling in osteoblasts.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 30 citations in OpenAlex.
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- A novel non-invasive approach monitoring skeletal stem cell function throughJournal of orthopaedic translation · 2026Article
- Advancements in bone organoids: perspectives on construction methodologies and application strategies.Journal of advanced research · 2026Review
- CSNK1D inhibition suppresses head and neck squamous cell carcinoma progression through SHH and PTCH1 pathway.Cell death & disease · 2025Article
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- Addressing osteoblast senescence: Molecular pathways and the frontier of anti-ageing treatments.Clinical and translational medicine · 2025Review
- Signaling Pathways Driving MSC Osteogenesis: Mechanisms, Regulation, and Translational Applications.International journal of molecular sciences · 2025Review
- Spatiotemporal application of small molecules in fracture healing.Biomaterials translational · 2025Review
- Insight into the Association between Slitrk Protein and Neurodevelopmental and Neuropsychiatric Conditions.Biomolecules · 2024Review
- Cell signaling and transcriptional regulation of osteoblast lineage commitment, differentiation, bone formation, and homeostasis.Cell discovery · 2024Review
- Schnurri-3 controls osteogenic fate of Adipoq-lineage progenitors in bone marrow.Journal of orthopaedic translation · 2024Article
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- Slitrk4 is required for the development of inhibitory neurons in the fear memory circuit of the lateral amygdala.Frontiers in molecular neuroscience · 2024Article
- MUC21: a new target for tumor treatment.Frontiers in oncology · 2024Review
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- Discovery of a Vertebral Skeletal Stem Cell Driving Spinal Metastases.Research square · 2023Article
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- Skeletal stem cells: origins, definitions, and functions in bone development and disease.Life medicine · 2022Review
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 2 countries.
Funding
Abstract
Hedgehog signaling is essential for bone formation, including functioning as a means for the growth plate to drive skeletal mineralization. However, the mechanisms regulating hedgehog signaling specifically in bone-forming osteoblasts are largely unknown. Here, we identified SLIT and NTRK-like protein-5(Slitrk5), a transmembrane protein with few identified functions, as a negative regulator of hedgehog signaling in osteoblasts. Slitrk5 is selectively expressed in osteoblasts and loss of Slitrk5 enhanced osteoblast differentiation in vitro and in vivo. Loss of SLITRK5 in vitro leads to increased hedgehog signaling and overexpression of SLITRK5 in osteoblasts inhibits the induction of targets downstream of hedgehog signaling. Mechanistically, SLITRK5 binds to hedgehog ligands via its extracellular domain and interacts with PTCH1 via its intracellular domain. SLITRK5 is present in the primary cilium, and loss of SLITRK5 enhances SMO ciliary enrichment upon SHH stimulation. Thus, SLITRK5 is a negative regulator of hedgehog signaling in osteoblasts that may be attractive as a therapeutic target to enhance bone formation.
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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.