ArticleBone2018
The YAP/TAZ transcriptional co-activators have opposing effects at different stages of osteoblast differentiation.
Article in Bone, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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
73 citing papers in PubMed, 112 citations in OpenAlex.
- Reprogramming bone homeostasis: The recoupling-oriented framework of bidirectional regulation strategies for osteoporosis.iScience · 2026Review
- Yap1 regulates motility and vertebral development and prevents kyphoscoliosis in zebrafish.PLoS genetics · 2026Article
- LATS1/2 Inhibitor Attenuates Osteoclast Differentiation via Hippo-YAP/TAZ Signaling Pathway and Alleviates Osteoporosis in Ovariectomized Rats.Current medical science · 2026Article
- Vascular Endothelial cell-derived Exosomal miR-5p-13348_267 Regulates the Fate Determination of Bone Marrow Mesenchymal Stem Cells (BMSCs).Cell biochemistry and biophysics · 2026Article
- Bone Metastasis in Estrogen Receptor-Positive Breast Cancer: Molecular Insights and Therapeutic Advances.International journal of molecular sciences · 2026Review
- Mechanical polarity as a driver of bone regeneration: a multiscale framework linking tension, mechanotransduction and cortical apposition.Frontiers in bioengineering and biotechnology · 2026Article
- Magnesium-containing implants enhance bone healing: A mechanobiological perspective.Mechanobiology in medicine · 2025Review
- Crosstalk between YAP/TAZ and ERα in mechanical and hormonal signaling in the skeletal system.Acta biochimica et biophysica Sinica · 2025Review
- PTH counteracts Hippo signaling via Src-dependent YAP stabilization to enhance bone marrow stromal cell differentiation.JCI insight · 2025Article
- Review
- Addressing osteoblast senescence: Molecular pathways and the frontier of anti-ageing treatments.Clinical and translational medicine · 2025Review
- Shaking culture attenuates circadian rhythms in induced pluripotent stem cells during osteogenic differentiation through the TEAD-Fbxl3-CRY axis.Cell death discovery · 2025Article
- Engineered bone-targeting apoptotic vesicles as a minimally invasive nanotherapy for heterotopic ossification.Journal of nanobiotechnology · 2025Article
- Metformin ameliorates osteoporosis by enhancing bone angiogenesis via the YAP1/TAZ-HIF1α axis.Molecular medicine (Cambridge, Mass.) · 2025Article
- Role of YAP/TAZ in bone diseases: A transductor from mechanics to biology.Journal of orthopaedic translation · 2025Review
- Extracellular matrix: Dystroglycan interactions-Roles for the dystrophin-associated glycoprotein complex in skeletal tissue dynamics.International journal of experimental pathology · 2025Review
- Review
- Deletion of the scavenger receptor Scarb1 in osteoblast progenitors and myeloid cells does not affect bone mass.PloS one · 2025Article
- Review
- Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The related transcriptional co-factors YAP (Yes-associated protein) and TAZ (transcriptional co-activator with PDZ-binding motif) have been proposed to either promote or inhibit osteoblast differentiation. Here we investigated the skeletal consequences of deleting YAP and TAZ at different stages of the osteoblast lineage using Prx1-Cre, Osx1-Cre, and Dmp1-Cre transgenic mice. Prx1-Cre-mediated deletion resulted in embryonic lethality. Mice lacking both copies of TAZ and one copy of YAP in cells targeted by Prx1-Cre were viable and displayed elevated bone mass associated increased bone formation. Deletion of YAP and TAZ using Osx1-Cre mice led to perinatal lethality. Suppression of Osx1-Cre activity until 21 days of age permitted postnatal deletion of YAP and TAZ, which resulted in increased osteoblast number at 12 weeks of age but no change in bone mass. Mechanistic studies revealed that YAP and TAZ suppress canonical Wnt signaling and Runx2 activity in osteoblast progenitors. Consistent with this, deletion of YAP and TAZ from osteoprogenitor cells increased osteoblast differentiation in vitro. Deletion of YAP and TAZ from mature osteoblasts and osteocytes using Dmp1-Cre mice led to reduced osteoblast number and bone formation, as well as increased osteoclast number, but no changes in known regulators of bone turnover such as RANKL, OPG, and Sost. Together these results suggest that YAP and TAZ in osteoblast progenitors oppose differentiation towards the osteoblast lineage but in mature osteoblasts and osteocytes, they promote bone formation and inhibit bone resorption.
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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.