Characterization of Kcnk3-Mutated Rat, a Novel Model of Pulmonary Hypertension.
暂无分享,去创建一个
M. Humbert | C. Péchoux | B. Girerd | F. Perros | D. Montani | T. Bertero | S. Remy | L. Tesson | I. Anegon | M. Nakhleh | C. Rücker-Martin | O. Mercier | B. Manoury | F. Antigny | M. Lambert | V. Capuano | A. Boet | A. Hautefort | V. Domergue | C. Rücker‐Martin
[1] M. Humbert,et al. Pathology and pathobiology of pulmonary hypertension: state of the art and research perspectives , 2019, European Respiratory Journal.
[2] Paul G. Williams,et al. Haemodynamic definitions and updated clinical classification of pulmonary hypertension , 2019, European Respiratory Journal.
[3] M. Humbert,et al. Ion Channels in Pulmonary Hypertension: A Therapeutic Interest? , 2018, International journal of molecular sciences.
[4] T. Bertero,et al. Factors Associated with Heritable Pulmonary Arterial Hypertension Exert Convergent Actions on the miR-130/301-Vascular Matrix Feedback Loop , 2018, International journal of molecular sciences.
[5] M. Mathier,et al. Serum albumin concentration as an independent prognostic indicator in patients with pulmonary arterial hypertension , 2018, Clinical cardiology.
[6] M. Humbert,et al. Loss of KCNK3 is a hallmark of RV hypertrophy/dysfunction associated with pulmonary hypertension , 2018, Cardiovascular research.
[7] J. Concordet,et al. Generation of gene-edited rats by delivery of CRISPR/Cas9 protein and donor DNA into intact zygotes using electroporation , 2017, Scientific Reports.
[8] M. Humbert,et al. TASK-1 (KCNK3) channels in the lung: from cell biology to clinical implications , 2017, European Respiratory Journal.
[9] M. Humbert,et al. T-type Ca2+ channels elicit pro-proliferative and anti-apoptotic responses through impaired PP2A/Akt1 signaling in PASMCs from patients with pulmonary arterial hypertension. , 2017, Biochimica et biophysica acta. Molecular cell research.
[10] S. Pullamsetti,et al. Vascular Stiffness and Mechanotransduction: Back in the Limelight. , 2017, American journal of respiratory and critical care medicine.
[11] M. Humbert,et al. Epidemiology and treatment of pulmonary arterial hypertension , 2017, Nature Reviews Cardiology.
[12] H. Date,et al. A burden of rare variants in BMPR2 and KCNK3 contributes to a risk of familial pulmonary arterial hypertension , 2017, BMC Pulmonary Medicine.
[13] P. Bayrak-Toydemir,et al. EIF2AK4 Mutations in Patients Diagnosed With Pulmonary Arterial Hypertension , 2017, Chest.
[14] S. Chai,et al. Contribution of two-pore K+ channels to cardiac ventricular action potential revealed using human iPSC-derived cardiomyocytes. , 2017, American journal of physiology. Heart and circulatory physiology.
[15] G. Murtaza,et al. TASK-1 potassium channel is not critically involved in mediating hypoxic pulmonary vasoconstriction of murine intra-pulmonary arteries , 2017, PloS one.
[16] P. Tejedor,et al. An homozygous mutation in KCNK3 is associated with an aggressive form of hereditary pulmonary arterial hypertension , 2017 .
[17] S. Archer,et al. MicroRNA‐138 and MicroRNA‐25 Down‐regulate Mitochondrial Calcium Uniporter, Causing the Pulmonary Arterial Hypertension Cancer Phenotype , 2017, American journal of respiratory and critical care medicine.
[18] V. Thongboonkerd,et al. Caveolae-mediated albumin transcytosis is enhanced in dengue-infected human endothelial cells: A model of vascular leakage in dengue hemorrhagic fever , 2016, Scientific Reports.
[19] C. Rhodes,et al. In Pulmonary Arterial Hypertension, Reduced BMPR2 Promotes Endothelial-to-Mesenchymal Transition via HMGA1 and Its Target Slug , 2016, Circulation.
[20] P. Newman,et al. Endothelial functions of platelet/endothelial cell adhesion molecule-1 (CD31) , 2016, Current opinion in hematology.
[21] M. Humbert,et al. Potassium Channel Subfamily K Member 3 (KCNK3) Contributes to the Development of Pulmonary Arterial Hypertension , 2016, Circulation.
[22] Juan Wang,et al. Hypoxia regulates ABCG2 activity through the activivation of ERK1/2/HIF-1α and contributes to chemoresistance in pancreatic cancer cells , 2016, Cancer biology & therapy.
[23] F. Perros,et al. Potassium channels in pulmonary arterial hypertension , 2015, European Respiratory Journal.
[24] M. Borggrefe,et al. Upregulation of K2P3.1 K+ Current Causes Action Potential Shortening in Patients With Chronic Atrial Fibrillation , 2015, Circulation.
[25] S. Archer,et al. Emerging Concepts in the Molecular Basis of Pulmonary Arterial Hypertension: Part I Metabolic Plasticity and Mitochondrial Dynamics in the Pulmonary Circulation and Right Ventricle in Pulmonary Arterial Hypertension , 2015, Circulation.
[26] M. Humbert,et al. Endothelial-to-Mesenchymal Transition in Pulmonary Hypertension , 2015, Circulation.
[27] Xian-Tao Li,et al. The Knockdown of TASK-1 Channels Improved the Proliferation of N2A Cells , 2015, Journal of Molecular Neuroscience.
[28] Lavannya M Pandit,et al. TWIK-2 Channel Deficiency Leads to Pulmonary Hypertension Through a Rho-Kinase–Mediated Process , 2014, Hypertension.
[29] W. Chung,et al. A novel channelopathy in pulmonary arterial hypertension. , 2013, The New England journal of medicine.
[30] P. Jurasz,et al. Hypoxia Results in Upregulation and De Novo Activation of Von Willebrand Factor Expression in Lung Endothelial Cells , 2013, Arteriosclerosis, thrombosis, and vascular biology.
[31] Cheng-ye Li,et al. Mitochondrial ROS-K+ channel signaling pathway regulated secretion of human pulmonary artery endothelial cells , 2012, Free radical research.
[32] A. Quyyumi,et al. Endothelium-Derived Hyperpolarizing Factor and Vascular Function , 2011, Cardiology research and practice.
[33] F. Sachse,et al. Knock-Out of the Potassium Channel TASK-1 Leads to a Prolonged QT Interval and a Disturbed QRS Complex , 2011, Cellular Physiology and Biochemistry.
[34] A. Gurney,et al. Contractile and electrophysiological properties of pulmonary artery smooth muscle are not altered in TASK‐1 knockout mice , 2011, The Journal of physiology.
[35] A. Malik,et al. Caveolin-1–eNOS signaling promotes p190RhoGAP-A nitration and endothelial permeability , 2011, The Journal of cell biology.
[36] S. Audi,et al. Quantifying mitochondrial and plasma membrane potentials in intact pulmonary arterial endothelial cells based on extracellular disposition of rhodamine dyes. , 2011, American journal of physiology. Lung cellular and molecular physiology.
[37] T. Kaneko,et al. Protein Kinase G Dynamically Modulates TASK1-Mediated Leak K+ Currents in Cholinergic Neurons of the Basal Forebrain , 2010, The Journal of Neuroscience.
[38] D. Bayliss,et al. TASK channel deletion in mice causes primary hyperaldosteronism , 2008, Proceedings of the National Academy of Sciences.
[39] D. Cane,et al. The nonsense-mediated decay RNA surveillance pathway. , 2007, Annual review of biochemistry.
[40] R. Barst,et al. von Willebrand factor independently predicts long-term survival in patients with pulmonary arterial hypertension. , 2005, Chest.
[41] J. Beavo,et al. Regulation of Nitric Oxide–Sensitive Guanylyl Cyclase Cyclic GMP Phosphodiesterases and Regulation of Smooth Muscle Function Structure, Regulation, and Function of Membrane Guanylyl Cyclase Receptors, With a Focus on GC-A Cyclic GMP–Dependent Protein Kinases and the Cardiovascular System: Insights F , 2003 .
[42] S. Archer,et al. The NO - K+ channel axis in pulmonary arterial hypertension. Activation by experimental oral therapies. , 2003, Advances in experimental medicine and biology.
[43] M. Frid,et al. Mature Vascular Endothelium Can Give Rise to Smooth Muscle Cells via Endothelial-Mesenchymal Transdifferentiation: In Vitro Analysis , 2002, Circulation research.
[44] M. Ueno,et al. Redox control of cell death. , 2002, Antioxidants & redox signaling.
[45] J. Dyck,et al. Dichloroacetate, a Metabolic Modulator, Prevents and Reverses Chronic Hypoxic Pulmonary Hypertension in Rats: Role of Increased Expression and Activity of Voltage-Gated Potassium Channels , 2002, Circulation.
[46] T. Beaty,et al. Impaired physiological responses to chronic hypoxia in mice partially deficient for hypoxia-inducible factor 1alpha. , 1999, The Journal of clinical investigation.
[47] V. Ingram,et al. Compromised mitochondrial function leads to increased cytosolic calcium and to activation of MAP kinases. , 1997, Proceedings of the National Academy of Sciences of the United States of America.