ArticleScientific reports2019
Structural consequences of BMPR2 kinase domain mutations causing pulmonary arterial hypertension.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 14 citations in OpenAlex.
- A rare recurring gain-of-function variant in BMPR2 causes neurodevelopmental phenotypes in humans and flies.American journal of human genetics · 2026Article
- Article
- Article
- Genetic screening in cohort of Egyptian patients with pulmonary arterial hypertension disease.Irish journal of medical science · 2025Article
- Cardiac Dysfunction in β-Thalassemia: A Narrative Review.Research in heart yield and translational medicine · 2025Review
- Therapeutic challenges and new therapeutic targets for combined capillary pulmonary hypertension: a review.Frontiers in medicine · 2025Review
- Design and Synthesis of Pyrazole-Based Macrocyclic Kinase Inhibitors Targeting BMPR2.ACS medicinal chemistry letters · 2023Article
- Identification of a novel mutation in the BMPR2 gene in a pulmonary arterial hypertension patient using next-generation sequencing.Journal of clinical laboratory analysis · 2022Article
- Article
- Fibroblast growth factors: the keepers of endothelial normalcy.The Journal of clinical investigation · 2021Article
- Structural basis for ALK2/BMPR2 receptor complex signaling through kinase domain oligomerization.Nature communications · 2021Article
- A Y-linked anti-Müllerian hormone type-II receptor is the sex-determining gene in ayu, Plecoglossus altivelis.PLoS genetics · 2021Article
- Review
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Bone morphogenetic proteins (BMPs) are secreted ligands of the transforming growth factor-β (TGF-β) family that control embryonic patterning, as well as tissue development and homeostasis. Loss of function mutations in the type II BMP receptor BMPR2 are the leading cause of pulmonary arterial hypertension (PAH), a rare disease of vascular occlusion that leads to high blood pressure in the pulmonary arteries. To understand the structural consequences of these mutations, we determined the crystal structure of the human wild-type BMPR2 kinase domain at 2.35 Å resolution. The structure revealed an active conformation of the catalytic domain that formed canonical interactions with the bound ligand Mg-ADP. Disease-associated missense mutations were mapped throughout the protein structure, but clustered predominantly in the larger kinase C-lobe. Modelling revealed that the mutations will destabilize the protein structure by varying extents consistent with their previously reported functional heterogeneity. The most severe mutations introduced steric clashes in the hydrophobic protein core, whereas those found on the protein surface were less destabilizing and potentially most favorable for therapeutic rescue strategies currently under clinical investigation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.