Associated Papers
The prevalence of pathogenic variants in the BMPR2 gene in patients with the idiopathic pulmonary arterial hypertension in the Russian population: sequencing data and meta-analysis.
Okhrimenko G et al.
Respiratory Research, 2025
40229839 (PubMed )
Supplement: 12931_2025_3214_MOESM2_ESM.xlsx › Assessment_
Genome scale analysis of pathogenic variants targetable for single base editing.
Lavrov AV et al.
Bmc Medical Genomics, 2020
32948190 (PubMed )
Supplement: 12920_2020_735_MOESM1_ESM.xlsx › mutations
Exome data clouds the pathogenicity of genetic variants in Pulmonary Arterial Hypertension.
Abbasi Y et al.
Molecular Genetics & Genomic Medicine, 2018
Identification of rare sequence variation underlying heritable pulmonary arterial hypertension.
Gräf S et al.
Nature Communications, 2018
29650961 (PubMed )
Supplement: 41467_2018_3672_MOESM1_ESM.xlsx › Suppl._Dataset_1
Clinical significance linked to functional defects in bone morphogenetic protein type 2 receptor, BMPR2.
Kim MJ et al.
Bmb Reports, 2017
Transforming growth factor-β(1) represses bone morphogenetic protein-mediated Smad signaling in pulmonary artery smooth muscle cells via Smad3.
Upton PD et al.
American Journal of Respiratory Cell and Molecular Biology, 2013
Mutations in bone morphogenetic protein type II receptor cause dysregulation of Id gene expression in pulmonary artery smooth muscle cells: implications for familial pulmonary arterial hypertension.
Yang J et al.
Circulation Research, 2008
BMP-dependent activation of caspase-9 and caspase-8 mediates apoptosis in pulmonary artery smooth muscle cells.
Lagna G et al.
American Journal of Physiology. Lung Cellular and Molecular Physiology, 2006
Mutations of the TGF-beta type II receptor BMPR2 in pulmonary arterial hypertension.
Machado RD et al.
Human Mutation, 2006
Dysfunctional Smad signaling contributes to abnormal smooth muscle cell proliferation in familial pulmonary arterial hypertension.
Yang X et al.
Circulation Research, 2005
Expression of mutant BMPR-II in pulmonary endothelial cells promotes apoptosis and a release of factors that stimulate proliferation of pulmonary arterial smooth muscle cells.
Yang X et al.
Pulmonary Circulation, 0
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