Insight into Molecular Mechanism for Activin A-Induced Bone Morphogenetic Protein Signaling

Investigating Protein–Protein Allosteric Network using Current‐Flow Scheme

(2019) Wesley M. Botello‐Smith et al.   JOURNAL OF COMPUTATIONAL CHEMISTRY

The Expansion of Heterotopic Bone in Fibrodysplasia Ossificans Progressiva Is Activin A-Dependent

(2017) Jaymin Upadhyay et al.   JOURNAL OF BONE AND MINERAL RESEARCH

Polymodal allosteric regulation of Type 1 Serine/Threonine Kinase Receptors via a conserved electrostatic lock

(2017) Wesley M. Botello-Smith et al.   PLoS Computational Biology

Activin A inhibits BMP-signaling by binding ACVR2A and ACVR2B

(2015) Oddrun Elise Olsen et al.   Cell Communication and Signaling

Mutant Activin-Like Kinase 2 in Fibrodysplasia Ossificans Progressiva are Activated via T203 by BMP Type II Receptors

(2015) Mai Fujimoto et al.   MOLECULAR ENDOCRINOLOGY

Neofunction of ACVR1 in fibrodysplasia ossificans progressiva

(2015) Kyosuke Hino et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

ACVR1 R206H receptor mutation causes fibrodysplasia ossificans progressiva by imparting responsiveness to activin A

(2015) Sarah J. Hatsell et al.   Science Translational Medicine

Constitutively Active ALK2 Receptor Mutants Require Type II Receptor Cooperation

(2013) J. Bagarova et al.   MOLECULAR AND CELLULAR BIOLOGY

Structure of the Bone Morphogenetic Protein Receptor ALK2 and Implications for Fibrodysplasia Ossificans Progressiva

(2012) Apirat Chaikuad et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

TGFβ signalling in context

(2012) Joan Massagué   NATURE REVIEWS MOLECULAR CELL BIOLOGY

In vitro Analyses of the Dysregulated R206H ALK2 Kinase-FKBP12 Interaction Associated with Heterotopic Ossification in FOP

(2011) Jay C. Groppe et al.   CELLS TISSUES ORGANS

Fibrodysplasia ossificans progressiva: Middle-age onset of heterotopic ossification from a unique missense mutation (c.974G > C, p.G325A) inACVR1

(2011) Michael P Whyte et al.   JOURNAL OF BONE AND MINERAL RESEARCH

A novel ACVR1 mutation in the glycine/serine-rich domain found in the most benign case of a fibrodysplasia ossificans progressiva variant reported to date

(2010) Celia L. Gregson et al.   BONE

Molecular Consequences of the ACVR1R206HMutation of Fibrodysplasia Ossificans Progressiva

(2010) Gin-Ah Song et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

TGF-β Superfamily Signaling in Embryonic Development and Homeostasis

(2009) Mary Y. Wu et al.   DEVELOPMENTAL CELL

ALK2 R206H Mutation Linked to Fibrodysplasia Ossificans Progressiva Confers Constitutive Activity to the BMP Type I Receptor and Sensitizes Mesenchymal Cells to BMP-Induced Osteoblast Differentiation and Bone Formation

(2009) Maarten van Dinther et al.   JOURNAL OF BONE AND MINERAL RESEARCH

The fibrodysplasia ossificans progressiva R206H ACVR1 mutation activates BMP-independent chondrogenesis and zebrafish embryo ventralization

(2009) Qi Shen et al.   JOURNAL OF CLINICAL INVESTIGATION

A unique case of fibrodysplasia ossificans progressiva with anACVR1 mutation, G356D, other than the common mutation (R206H)

(2008) Hirokazu Furuya et al.   AMERICAN JOURNAL OF MEDICAL GENETICS PART A

Mutational analysis of the ACVR1 gene in Italian patients affected with fibrodysplasia ossificans progressiva: confirmations and advancements

(2008) Renata Bocciardi et al.   EUROPEAN JOURNAL OF HUMAN GENETICS

Classic and atypical fibrodysplasia ossificans progressiva (FOP) phenotypes are caused by mutations in the bone morphogenetic protein (BMP) type I receptor ACVR1

(2008) Frederick S. Kaplan et al.   HUMAN MUTATION