Rosiglitazone suppresses RANKL‐induced NFATc1 autoamplification by disrupting the physical interaction between NFATc1 and PPARγ
Author:
Affiliation:
1. Department of Dentistry Kosin University Gospel Hospital Seo‐gu Korea
2. Department of Physiology Kosin University College of Medicine Seo‐gu Korea
3. Department of Pathology Kosin University College of Medicine Seo‐gu Korea
Funder
College of Medicine, Koisin University
Publisher
Wiley
Subject
General Biochemistry, Genetics and Molecular Biology
Link
https://onlinelibrary.wiley.com/doi/pdf/10.1002/2211-5463.12513
Reference36 articles.
1. Receptor Activator of Nuclear Factor-κB Ligand Activates Nuclear Factor-κB in Osteoclast Precursors*
2. The Calcineurin/Nuclear Factor of Activated T Cells Signaling Pathway Regulates Osteoclastogenesis in RAW264.7 Cells
3. Induction and Activation of the Transcription Factor NFATc1 (NFAT2) Integrate RANKL Signaling in Terminal Differentiation of Osteoclasts
4. Autoamplification of NFATc1 expression determines its essential role in bone homeostasis
5. NFATc1 in mice represses osteoprotegerin during osteoclastogenesis and dissociates systemic osteopenia from inflammation in cherubism
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3. Peroxisome Proliferator-Activated Receptor-γ Antagonizes LOX-1-Mediated Endothelial Injury by Transcriptional Activation of miR-590-5p;PPAR Research;2019-07-01
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