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American Journal of Medical Genetics. Part A|April 24, 2019
Severe digital malformations in a rare variant of fibrodysplasia ossificans progressivaZoran Gucev, Velibor Tasic, Dijana Plaseska-Karanfilska, et al.
Bioorganic & Medicinal Chemistry Letters|December 27, 2015
α-Aryl pyrrolidine sulfonamides as TRPA1 antagonistsVishal A Verma, Daniel G M Shore, Huifen Chen, et al.
Human Molecular Genetics|May 24, 2014
ACVR1 p.Q207E causes classic fibrodysplasia ossificans progressiva and is functionally distinct from the engineered constitutively active ACVR1 p.Q207D variantJulia Haupt, Alexandra Deichsel, Katja Stange, et al.
The New England Journal of Medicine|January 11, 2002
Paternally inherited inactivating mutations of the GNAS1 gene in progressive osseous heteroplasiaEileen M Shore, Jaimo Ahn, Suzanne Jan de Beur, et al.
Women'S Health Issues : Official Publication of the Jacobs Institute of Women'S Health|July 9, 2025
Patterns of Antepartum Care in Ontario Before and During a Time of COVID-19 and Virtual Care: A Population-Based StudyStephanie C Lapinsky, Nancy N Baxter, Rinku Sutradhar, et al.
Pediatric Blood & Cancer|May 27, 2015
Treatment of neuroblastoma in congenital central hypoventilation syndrome with a PHOX2B polyalanine repeat expansion mutation: New twist on a neurocristopathy syndromeAmy E Armstrong, Debra E Weese-Mayer, Amir Mian, et al.
Journal of Neurology|June 28, 2012
CNS demyelination in fibrodysplasia ossificans progressivaLixin Kan, Joseph A Kitterman, Daniele Procissi, et al.
American Journal of Human Genetics|January 13, 2000
Fibrodysplasia ossificans progressiva, a heritable disorder of severe heterotopic ossification, maps to human chromosome 4q27-31G Feldman, M Li, S Martin, et al.
Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research|March 31, 2016
Cellular Hypoxia Promotes Heterotopic Ossification by Amplifying BMP SignalingHaitao Wang, Carter Lindborg, Vitali Lounev, et al.
Biomolecules|July 29, 2023
Polypeptide Substrate Accessibility Hypothesis: Gain-of-Function R206H Mutation Allosterically Affects Activin Receptor-like Protein Kinase ActivityJay C Groppe, Guorong Lu, Mary R Tandang-Silvas, et al.
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