ArticleThe Journal of clinical investigation2011
3BP2-deficient mice are osteoporotic with impaired osteoblast and osteoclast functions.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01630447 (Identification of Mutations That Lead to Cherubism in Families and Isolated Cases and Studies of Cellular and Molecular Mechanisms), which is not on this map. Cited by 43 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Identification of Mutations That Lead to Cherubism in Families and Isolated Cases and Studies of Cellular and Molecular Mechanisms
Who cites it
43 citing papers in PubMed, 73 citations in OpenAlex.
- Comparative analysis of osteoclast function in symptomatic and asymptomatic individuals with cherubism-causing SH3BP2 mutation.JBMR plus · 2025Article
- Silencing of SH3BP2 Inhibits Microglia Activation Via the JAK/STAT Signaling in Spinal Cord Injury Models.Inflammation · 2025Article
- PARylation-mediated post-transcriptional modifications in cancer immunity and immunotherapy.Frontiers in immunology · 2025Review
- Apocynin exerts cytoprotective effects on dexamethasone-induced osteoblasts by inhibiting oxidative stress through the Nrf2 signalling pathway.Journal of cellular and molecular medicine · 2023Article
- E3-ubiquitin ligases and recent progress in osteoimmunology.Frontiers in immunology · 2023Review
- Tankyrase represses autoinflammation through the attenuation of TLR2 signaling.The Journal of clinical investigation · 2022Article
- Wnt/β-catenin signaling in cancers and targeted therapies.Signal transduction and targeted therapy · 2021Review
- Repair calvarial defect of osteoporotic rats by berberine functionalized porous calcium phosphate scaffold.Regenerative biomaterials · 2021Article
- RUNX2 Phosphorylation by Tyrosine Kinase ABL Promotes Breast Cancer Invasion.Frontiers in oncology · 2021Article
- The Potential Role of RP105 in Regulation of Inflammation and Osteoclastogenesis During Inflammatory Diseases.Frontiers in cell and developmental biology · 2021Review
- Cherubism as a systemic skeletal disease: evidence from an aggressive case.BMC musculoskeletal disorders · 2020Article
- Article
- Alveolar Bone Protection by Targeting the SH3BP2-SYK Axis in Osteoclasts.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020Article
- Role of osteoclasts in oral homeostasis and jawbone diseases.Oral science international · 2020Article
- Poly(ADP-ribose) polymerase enzymes and the maintenance of genome integrity.Cellular and molecular life sciences : CMLS · 2020Review
- Review
- Use of Denosumab in Children With Osteoclast Bone Dysplasias: Report of Three Cases.JBMR plus · 2019Article
- Article
- Tankyrase (PARP5) Inhibition Induces Bone Loss through Accumulation of Its Substrate SH3BP2.Cells · 2019Review
- Osteoimmunology.Cold Spring Harbor perspectives in medicine · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A fine balance between bone resorption by osteoclasts and bone formation by osteoblasts maintains bone homeostasis. In patients with cherubism, gain-of-function mutations in 3BP2, which is encoded by SH3-domain binding protein 2 (SH3BP2), cause cystic lesions with activated osteoclasts that lead to craniofacial abnormalities. However, little is known about the function of wild-type 3BP2 in regulating bone homeostasis. Here we have shown that 3BP2 is required for the normal function of both osteoblasts and osteoclasts. Initial analysis showed that Sh3bp2-/-mice developed osteoporosis as a result of reduced bone formation despite the fact that bone resorption was impaired. We demonstrated using reciprocal bone marrow chimeras, a cell-intrinsic defect of the osteoblast and osteoclast compartments in vivo. Further, Sh3bp2-/- osteoblasts failed to mature and form mineralized nodules in vitro, while Sh3bp2-/- osteoclasts spread poorly and were unable to effectively degrade dentine matrix in vitro. Finally, we showed that 3BP2 was required for Abl activation in osteoblasts and Src activation in osteoclasts, and demonstrated that the in vitro defect of each cell type was restored by the respective expression of activated forms of these kinases. These findings reveal an unanticipated role for the 3BP2 adapter protein in osteoblast function and in coordinating bone homeostatic signals in both osteoclast and osteoblast lineages.
Indexed as
Identifiers
What OpenQuestion holds
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.