ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Identification of NIBAN2-Regulated RUNX2 Alternative Splicing Presents Novel Strategies for Antagonizing Osteoporosis.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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.
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Who cites it
8 citing papers in PubMed.
- Ceramide-PKCζ signaling axis mediates burn-enhanced ectopic calcification during Achilles tendon healing.Journal of molecular histology · 2026Article
- Integrative multiomic analysis reveals co-ordinated alternative splicing in human bone marrow stromal stem cells.Scientific reports · 2026Article
- Recapitulating Endochondral Ossification for Bone Repair: From Development to Engineering Strategy.Advanced healthcare materials · 2026Review
- NIBAN2/FLII/RREB1 Axis Drives Glioma Stem Cell Malignancy via TLR3 Pathway Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Estrogen promotes the angiogenesis and osteogenesis of bone marrow stromal cells via regulating ESR1/RUNX2 axis.Food & nutrition research · 2026Article
- Alternative Splicing: Molecular Mechanisms, Biological Functions, Diseases, and Potential Therapeutic Targets.MedComm · 2025Review
- Identification of NIBAN2-Regulated RUNX2 Alternative Splicing Presents Novel Strategies for Antagonizing Osteoporosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Alternative Splicing: A Critical Regulator in Human Bone Biology and Tumor Progression.Research (Washington, D.C.) · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Osteoporosis is characterized by excessive bone resorption and/or defects in bone formation. Identification of factors promoting osteoblast differentiation may provide potential targets for osteoporosis therapy. Through integral analyses of multiple datasets, NIBAN2 is found to be tightly associated with bone formation and osteoporosis. Indeed, NIBAN2 promotes osteoblast differentiation, and conditional Niban2 knockout in osteoblasts caused bone loss and insufficient mineralization. Mechanistically, NIBAN2 interacts with the HNRNPU-cored spliceosome complex and alters its components to regulate the alternative splicing of RUNX2, which ultimately cause an increase in functional RUNX2 (nuclear localization sequence complete) but a decrease in dysfunctional RUNX2 (exon 6 exclusive) to reinforce osteoblast differentiation. Most importantly, NIBAN2 expression level negatively correlates with RUNX2 spliced isoforms and bone loss in osteoporosis patients. NIBAN2 overexpression rescues bone loss in ovariectomized mice. Thus, this research identifies NIBAN2-regulated RUNX2 alternative splicing as a potential mechanism of osteoblast differentiation that may present strategies for antagonizing 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.