Bone Morphogenetic Protein Receptor-2 and Pulmonary Arterial Hypertension

This publication has 18 references indexed in Scilit:

• Dysfunctional Smad Signaling Contributes to Abnormal Smooth Muscle Cell Proliferation in Familial Pulmonary Arterial Hypertension
  Circulation Research, 2005
• Pathogenesis of Pulmonary Arterial Hypertension
  Circulation, 2005
• Pulmonary Hypertension in Transgenic Mice Expressing a Dominant-Negative BMPRII Gene in Smooth Muscle
  Circulation Research, 2004
• Smad-dependent and Smad-independent pathways in TGF-β family signalling
  Nature, 2003
• Mechanisms of TGF-β Signaling from Cell Membrane to the Nucleus
  Cell, 2003
• Suppression of Tumor Necrosis Factor-mediated Apoptosis by Nuclear Factor κB-independent Bone Morphogenetic Protein/Smad Signaling
  Published by Elsevier ,2001
• Bone Morphogenetic Protein-2 Inhibits Serum Deprivation-induced Apoptosis of Neonatal Cardiac Myocytes through Activation of the Smad1 Pathway
  Journal of Biological Chemistry, 2001
• Inhibition of the VEGF receptor 2 combined with chronic hypoxia causes cell death‐dependent pulmonary endothelial cell proliferation and severe pulmonary hypertension
  The FASEB Journal, 2001
• Sporadic primary pulmonary hypertension is associated with germline mutations of the gene encoding BMPR-II, a receptor member of the TGF-beta family
  Journal of Medical Genetics, 2000
• Monoclonal endothelial cell proliferation is present in primary but not secondary pulmonary hypertension.
  Journal of Clinical Investigation, 1998