Associated Papers
Molecular insights into TGF-B signalling pathway disruption by non-synonymous SNPs variants in COPD: an in silico and molecular dynamics simulation study.
Mahajan N et al.
Journal of Biomolecular Structure & Dynamics, 2025
Therapeutic potential of allosteric HECT E3 ligase inhibition.
Rothman AMK et al.
Cell, 2025
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
Adaptation of ACMG/AMP Guidelines for Clinical Classification of BMPR2 Variants in Pulmonary Arterial Hypertension Resolves Variants of Unclear Pathogenicity in ClinVar.
Eichstaedt CA et al.
Human Mutation, 2025
Adaptation of ACMG/AMP guidelines for clinical classification of BMPR2 variants in Pulmonary Arterial Hypertension resolves variants of unclear pathogenicity in ClinVar.
Eichstaedt CA et al.
Medrxiv : the Preprint Server for Health Sciences, 2024
Molecular and Genetic Profiling for Precision Medicines in Pulmonary Arterial Hypertension.
Fazal S et al.
Cells, 2021
Structural consequences of BMPR2 kinase domain mutations causing pulmonary arterial hypertension.
Chaikuad A et al.
Scientific Reports, 2019
Exome data clouds the pathogenicity of genetic variants in Pulmonary Arterial Hypertension.
Abbasi Y et al.
Molecular Genetics & Genomic Medicine, 2018
Clinical significance linked to functional defects in bone morphogenetic protein type 2 receptor, BMPR2.
Kim MJ et al.
Bmb Reports, 2017
Sequencing of mutations in the serine/threonine kinase domain of the bone morphogenetic protein receptor type 2 gene causing pulmonary arterial hypertension.
Mutlu Z et al.
Anatolian Journal of Cardiology, 2016
Id proteins are critical downstream effectors of BMP signaling in human pulmonary arterial smooth muscle cells.
Yang J et al.
American Journal of Physiology. Lung Cellular and Molecular Physiology, 2013
Inhibition of overactive transforming growth factor-β signaling by prostacyclin analogs in pulmonary arterial hypertension.
Ogo T et al.
American Journal of Respiratory Cell and Molecular Biology, 2013
Sildenafil potentiates bone morphogenetic protein signaling in pulmonary arterial smooth muscle cells and in experimental pulmonary hypertension.
Yang J et al.
Arteriosclerosis, Thrombosis, and Vascular Biology, 2013
Smad-dependent and smad-independent induction of id1 by prostacyclin analogues inhibits proliferation of pulmonary artery smooth muscle cells in vitro and in vivo.
Yang J et al.
Circulation Research, 2010
Stoichiometric imbalance in the receptor complex contributes to dysfunctional BMPR-II mediated signalling in pulmonary arterial hypertension.
Nasim MT et al.
Human Molecular Genetics, 2008
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
Functional analysis of bone morphogenetic protein type II receptor mutations underlying primary pulmonary hypertension.
Rudarakanchana N et al.
Human Molecular Genetics, 2002
Heterozygous germline mutations in BMPR2, encoding a TGF-beta receptor, cause familial primary pulmonary hypertension.
Lane KB et al.
Nature Genetics, 2000