The obligatory role of Activin A in the formation of heterotopic bone in Fibrodysplasia Ossificans Progressiva
Open Access
- 16 June 2017
- journal article
- review article
- Published by Elsevier BV in Bone
- Vol. 109, 210-217
- https://doi.org/10.1016/j.bone.2017.06.011
Abstract
No abstract availableKeywords
This publication has 72 references indexed in Scilit:
- A New Class of Small Molecule Inhibitor of BMP SignalingPLOS ONE, 2013
- Multipotent progenitors resident in the skeletal muscle interstitium exhibit robust BMP-dependent osteogenic activity and mediate heterotopic ossificationJournal of Bone and Mineral Research, 2012
- Restoration of normal BMP signaling levels and osteogenic differentiation in FOP mesenchymal progenitor cells by mutant allele-specific targetingGene Therapy, 2011
- Potent inhibition of heterotopic ossification by nuclear retinoic acid receptor-γ agonistsNature Medicine, 2011
- A novel ACVR1 mutation in the glycine/serine-rich domain found in the most benign case of a fibrodysplasia ossificans progressiva variant reported to dateBone, 2011
- Conversion of vascular endothelial cells into multipotent stem-like cellsNature Medicine, 2010
- Inherited human diseases of heterotopic bone formationNature Reviews Rheumatology, 2010
- Characterization of the Ligand Binding Functionality of the Extracellular Domain of Activin Receptor Type IIBPublished by Elsevier BV ,2010
- Classic and atypical fibrodysplasia ossificans progressiva (FOP) phenotypes are caused by mutations in the bone morphogenetic protein (BMP) type I receptor ACVR1Human Mutation, 2008
- BMP type I receptor inhibition reduces heterotopic ossificationNature Medicine, 2008