Tolvaptan activates the Nrf2/HO-1 antioxidant pathway through PERK phosphorylation

[1]  S. Sasaki,et al.  AKAPs-PKA disruptors increase AQP2 activity independently of vasopressin in a model of nephrogenic diabetes insipidus , 2018, Nature Communications.

[2]  S. Uchida,et al.  Activation of AQP2 water channels without vasopressin: therapeutic strategies for congenital nephrogenic diabetes insipidus , 2018, Clinical and Experimental Nephrology.

[3]  D. McGill,et al.  Tolvaptan for Heart Failure in Chronic Kidney Disease Patients: A Systematic Review and Meta-Analysis. , 2018, Heart, lung & circulation.

[4]  Glenn M. Chertow,et al.  Bardoxolone Methyl Improves Kidney Function in Patients with Chronic Kidney Disease Stage 4 and Type 2 Diabetes: Post-Hoc Analyses from Bardoxolone Methyl Evaluation in Patients with Chronic Kidney Disease and Type 2 Diabetes Study , 2018, American Journal of Nephrology.

[5]  M. Lanaspa,et al.  Novel treatment strategies for chronic kidney disease: insights from the animal kingdom , 2018, Nature Reviews Nephrology.

[6]  E. Pistikopoulos,et al.  In vitro Studies. , 2017 .

[7]  Masayuki Yamamoto,et al.  Targeting the KEAP1-NRF2 System to Prevent Kidney Disease Progression , 2017, American Journal of Nephrology.

[8]  Pieter Beerepoot,et al.  Pharmacological chaperone approaches for rescuing GPCR mutants: Current state, challenges, and screening strategies , 2017, Pharmacological research.

[9]  S. Ito,et al.  Transcription factor Nrf2 hyperactivation in early-phase renal ischemia-reperfusion injury prevents tubular damage progression. , 2017, Kidney international.

[10]  S. Sasaki,et al.  Wnt5a induces renal AQP2 expression by activating calcineurin signalling pathway , 2016, Nature Communications.

[11]  M. Ferrer,et al.  Small Molecule Inhibitor of NRF2 Selectively Intervenes Therapeutic Resistance in KEAP1-Deficient NSCLC Tumors. , 2016, ACS chemical biology.

[12]  V. Morwitz.  Insights from the Animal Kingdom , 2014 .

[13]  Yongfang Jiang,et al.  Therapeutic targeting of GSK3β enhances the Nrf2 antioxidant response and confers hepatic cytoprotection in hepatitis C , 2014, Gut.

[14]  N. Vaziri,et al.  The synthetic triterpenoid RTA dh404 (CDDO-dhTFEA) restores Nrf2 activity and attenuates oxidative stress, inflammation, and fibrosis in rats with chronic kidney disease , 2013, Xenobiotica; the fate of foreign compounds in biological systems.

[15]  V. Torres,et al.  Strategies targeting cAMP signaling in the treatment of polycystic kidney disease. , 2014, Journal of the American Society of Nephrology : JASN.

[16]  J. McMurray,et al.  Bardoxolone methyl in type 2 diabetes and stage 4 chronic kidney disease. , 2013, The New England journal of medicine.

[17]  Keith C. Norris,et al.  Role of impaired Nrf2 activation in the pathogenesis of oxidative stress and inflammation in chronic tubulo-interstitial nephropathy. , 2013, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.

[18]  H. Nishitoh,et al.  Signaling Pathways from the Endoplasmic Reticulum and Their Roles in Disease , 2013, Genes.

[19]  M. Ishikawa,et al.  Renoprotective effect of vasopressin v2 receptor antagonist tolvaptan in Dahl rats with end-stage heart failure. , 2013, International heart journal.

[20]  Eiji Higashihara,et al.  Tolvaptan in patients with autosomal dominant polycystic kidney disease. , 2012, The New England journal of medicine.

[21]  P. Ray,et al.  Reactive oxygen species (ROS) homeostasis and redox regulation in cellular signaling. , 2012, Cellular signalling.

[22]  Kazuhiro Takahashi,et al.  V2 Vasopressin Receptor (V2R) Mutations in Partial Nephrogenic Diabetes Insipidus Highlight Protean Agonism of V2R Antagonists* , 2011, The Journal of Biological Chemistry.

[23]  Tadashi Senba,et al.  Nonclinical Safety Profile of Tolvaptan , 2011, Cardiovascular Drugs and Therapy.

[24]  Philip Raskin,et al.  Bardoxolone methyl and kidney function in CKD with type 2 diabetes. , 2011, The New England journal of medicine.

[25]  H. J. Kim,et al.  Role of Intrarenal Angiotensin System Activation, Oxidative Stress, Inflammation, and Impaired Nuclear Factor-Erythroid-2-Related Factor 2 Activity in the Progression of Focal Glomerulosclerosis , 2011, Journal of Pharmacology and Experimental Therapeutics.

[26]  H. J. Kim,et al.  Contribution of impaired Nrf2-Keap1 pathway to oxidative stress and inflammation in chronic renal failure. , 2010, American journal of physiology. Renal physiology.

[27]  Xinmin Zhang,et al.  The IRE1alpha-XBP1 pathway of the unfolded protein response is required for adipogenesis. , 2009, Cell metabolism.

[28]  H. Kawachi,et al.  Tolvaptan, a selective oral vasopressin V2 receptor antagonist, ameliorates podocyte injury in puromycin aminonucleoside nephrotic rats , 2009, Clinical and Experimental Nephrology.

[29]  W. Müller-Esterl,et al.  Vasopressin V2 receptor expression along rat, mouse, and human renal epithelia with focus on TAL. , 2007, American journal of physiology. Renal physiology.

[30]  H. Shibuya,et al.  Molecular pathogenesis of pseudohypoaldosteronism type II: generation and analysis of a Wnk4(D561A/+) knockin mouse model. , 2007, Cell metabolism.

[31]  T. Berl,et al.  Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia. , 2006, The New England journal of medicine.

[32]  A. Sanabria,et al.  Randomized controlled trial. , 2005, World journal of surgery.

[33]  Paul Talalay,et al.  Extremely potent triterpenoid inducers of the phase 2 response: correlations of protection against oxidant and inflammatory stress. , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[34]  S. Reddy,et al.  NADPH Oxidase and ERK Signaling Regulates Hyperoxia-induced Nrf2-ARE Transcriptional Response in Pulmonary Epithelial Cells* , 2004, Journal of Biological Chemistry.

[35]  Michel Bouvier,et al.  Functional rescue of the constitutively internalized V2 vasopressin receptor mutant R137H by the pharmacological chaperone action of SR49059. , 2004, Molecular endocrinology.

[36]  C. O'connor,et al.  Effects of Tolvaptan, a Vasopressin Antagonist, in Patients Hospitalized with Worsening Heart Failure: A Randomized Controlled Trial , 2004 .

[37]  A. I. Rojo,et al.  Regulation of Heme Oxygenase-1 Expression through the Phosphatidylinositol 3-Kinase/Akt Pathway and the Nrf2 Transcription Factor in Response to the Antioxidant Phytochemical Carnosol* , 2004, Journal of Biological Chemistry.

[38]  Randal J. Kaufman,et al.  Nrf2 Is a Direct PERK Substrate and Effector of PERK-Dependent Cell Survival , 2003, Molecular and Cellular Biology.

[39]  M. Iezzi,et al.  Desmopressin (DDAVP) induces NO production in human endothelial cells via V2 receptor‐ and cAMP‐mediated signaling , 2003, Journal of thrombosis and haemostasis : JTH.

[40]  H. Huang,et al.  Increased Protein Stability as a Mechanism That Enhances Nrf2-mediated Transcriptional Activation of the Antioxidant Response Element , 2003, The Journal of Biological Chemistry.

[41]  T. Tsuruo,et al.  Modulation of Akt kinase activity by binding to Hsp90. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[42]  A. Kahn,et al.  Corticosteroid-dependent sodium transport in a novel immortalized mouse collecting duct principal cell line. , 1999, Journal of the American Society of Nephrology : JASN.

[43]  D. Ron,et al.  Protein translation and folding are coupled by an endoplasmic-reticulum-resident kinase , 1999, Nature.

[44]  J. D. Engel,et al.  Keap1 represses nuclear activation of antioxidant responsive elements by Nrf2 through binding to the amino-terminal Neh2 domain. , 1999, Genes & development.

[45]  C. S. Gal,et al.  Characterization of SR 121463A, a highly potent and selective, orally active vasopressin V2 receptor antagonist. , 1996, The Journal of clinical investigation.

[46]  J. Bertram,et al.  Reactive oxygen species in puromycin aminonucleoside nephrosis: in vitro studies. , 1994, Kidney international.

[47]  Nancy Y. Ip,et al.  ERKs: A family of protein-serine/threonine kinases that are activated and tyrosine phosphorylated in response to insulin and NGF , 1991, Cell.