ArticleThe Journal of clinical investigation2013
Schnurri-3 regulates ERK downstream of WNT signaling in osteoblasts.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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.
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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
44 citing papers in PubMed, 66 citations in OpenAlex.
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- Viridicatol from the Deep-Sea-Derived Fungus Alleviates Bone Loss by Targeting the Wnt/SHN3 Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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- Engineering a targeted and safe bone anabolic gene therapy to treat osteoporosis in alveolar bone loss.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Schnurri-3 inhibition rescues skeletal fragility and vascular skeletal stem cell niche pathology in the OIM model of osteogenesis imperfecta.Bone research · 2024Article
- Bone controls browning of white adipose tissue and protects from diet-induced obesity through Schnurri-3-regulated SLIT2 secretion.Nature communications · 2024Article
- Advances in Bone-Targeting Drug Delivery: Emerging Strategies Using Adeno-Associated Virus.Human gene therapy · 2024Review
- Schnurri-3 controls osteogenic fate of Adipoq-lineage progenitors in bone marrow.Journal of orthopaedic translation · 2024Article
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- Schnurri-3 inhibition suppresses bone and joint damage in models of rheumatoid arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- WNT-modulating gene silencers as a gene therapy for osteoporosis, bone fracture, and critical-sized bone defects.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Discovery of a Vertebral Skeletal Stem Cell Driving Spinal Metastases.Research square · 2023Article
- Unveiling the common loci for six body measurement traits in Chinese Wenshan cattle.Frontiers in genetics · 2023Article
- Application and Molecular Mechanisms of Extracellular Vesicles Derived from Mesenchymal Stem Cells in Osteoporosis.Current issues in molecular biology · 2022Review
- Article
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 1 country.
Funding
Abstract
Mice deficient in Schnurri-3 (SHN3; also known as HIVEP3) display increased bone formation, but harnessing this observation for therapeutic benefit requires an improved understanding of how SHN3 functions in osteoblasts. Here we identified SHN3 as a dampener of ERK activity that functions in part downstream of WNT signaling in osteoblasts. A D-domain motif within SHN3 mediated the interaction with and inhibition of ERK activity and osteoblast differentiation, and knockin of a mutation in Shn3 that abolishes this interaction resulted in aberrant ERK activation and consequent osteoblast hyperactivity in vivo. Additionally, in vivo genetic interaction studies demonstrated that crossing to Lrp5(-/-) mice partially rescued the osteosclerotic phenotype of Shn3(-/-) mice; mechanistically, this corresponded to the ability of SHN3 to inhibit ERK-mediated suppression of GSK3β. Inducible knockdown of Shn3 in adult mice resulted in a high-bone mass phenotype, providing evidence that transient blockade of these pathways in adults holds promise as a therapy for osteoporosis.
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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.