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Article

Overexpression of Wild-Type ACVR1 in Fibrodysplasia Ossificans Progressiva Mice Rescues Perinatal Lethality and Inhibits Heterotopic Ossification.

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research - 1 Nov 2022

Yamamoto Masakazu, Stoessel Sean J, Yamamoto Shoko, Goldhamer David J

Abstract excerpt

Fibrodysplasia ossificans progressiva (FOP) is a devastating disease of progressive heterotopic bone formation for which effective treatments are currently unavailable. FOP is caused by dominant gain-of-function mutations in the receptor ACVR1 (also known as ALK2), which render the receptor inappropriately responsive to activin ligands. In previous studies, we developed a genetic mouse model of FOP that...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 35637634
DOI: 10.1002/jbmr.4617
PMCID: PMC9708949

Genes

ACVR1

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Overexpression of Wild-Type ACVR1 in Fibrodysplasia Ossificans Progressiva Mice Rescues Perinatal Lethality and Inhibits Heterotopic Ossification.PMID 35637634Read ↗

Over-expression of wild-type <i>ACVR1</i> in fibrodysplasia ossificans progressiva mice rescues perinatal lethality and inhibits heterotopic ossificationSemantic proximity Read ↗

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Activin-dependent signaling in fibro/adipogenic progenitors causes fibrodysplasia ossificans progressivaSemantic proximity Read ↗

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ACVR1R206H receptor mutation causes fibrodysplasia ossificans progressiva by imparting responsiveness to activin A.Semantic proximity Read ↗

Anti-ACVR1 antibodies exacerbate heterotopic ossification in fibrodysplasia ossificans progressiva (FOP) by activating FOP-mutant ACVR1.Semantic proximity Read ↗

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