Associated Papers
Human iPSCs as Model Systems for BMP-Related Rare Diseases.
Sánchez-Duffhues G et al.
Cells, 2023
Multi-omics therapeutic perspective on ACVR1 gene: from genetic alterations to potential targeting.
Nagar G et al.
Briefings in Functional Genomics, 2023
Accumulated Knowledge of Activin Receptor-Like Kinase 2 (ALK2)/Activin A Receptor, Type 1 (ACVR1) as a Target for Human Disorders.
Katagiri T et al.
Biomedicines, 2021
Cardiopulmonary and Neurologic Dysfunctions in Fibrodysplasia Ossificans Progressiva.
Khan F et al.
Biomedicines, 2021
Design of primers for direct sequencing of nine coding exons in the human ACVR1 gene.
Matsuoka M et al.
Bone, 2020
Bone morphogenetic protein receptors: Structure, function and targeting by selective small molecule kinase inhibitors.
Sanchez-Duffhues G et al.
Bone, 2020
Patients with ACVR1R206H mutations have an increased prevalence of cardiac conduction abnormalities on electrocardiogram in a natural history study of Fibrodysplasia Ossificans Progressiva.
Kou S et al.
Orphanet Journal of Rare Diseases, 2020
Effects of FKBP12 and type II BMP receptors on signal transduction by ALK2 activating mutations associated with genetic disorders.
Machiya A et al.
Bone, 2018
Heterotopic bone induction via BMP signaling: Potential therapeutic targets for fibrodysplasia ossificans progressiva.
Katagiri T et al.
Bone, 2018
Mutant activin-like kinase 2 in fibrodysplasia ossificans progressiva are activated via T203 by BMP type II receptors.
Fujimoto M et al.
Molecular Endocrinology (baltimore, Md.), 2015
AcvR1-mediated BMP signaling in second heart field is required for arterial pole development: implications for myocardial differentiation and regional identity.
Thomas PS et al.
Developmental Biology, 2014
Genetic factors in non-syndromic congenital heart malformations.
Wessels MW et al.
Clinical Genetics, 2010
Genetics of congenital heart defects: a candidate gene approach.
Lagendijk AK et al.
Trends in Cardiovascular Medicine, 2010
Dominant-negative ALK2 allele associates with congenital heart defects.
Smith KA et al.
Circulation, 2009
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