Pharmacologic ATF6 activation confers global protection in widespread disease models by reprograming cellular proteostasis

[1]  Cathy James-Springer,et al.  Challenges and Future Opportunities , 2021, A Tool for Determining e-Learning Readiness.

[2]  S. Hernandez-Resendiz,et al.  The Role of Redox Dysregulation in the Inflammatory Response to Acute Myocardial Ischaemia-reperfusion Injury - Adding Fuel to the Fire. , 2017, Current medicinal chemistry.

[3]  Alan D. Lopez,et al.  Global, Regional, and National Burden of Cardiovascular Diseases for 10 Causes, 1990 to 2015 , 2017, Journal of the American College of Cardiology.

[4]  P. Ping,et al.  HSPA5 Gene encoding Hsp70 chaperone BiP in the endoplasmic reticulum. , 2017, Gene.

[5]  M. Gillum,et al.  ER Stress Inhibits Liver Fatty Acid Oxidation while Unmitigated Stress Leads to Anorexia-Induced Lipolysis and Both Liver and Kidney Steatosis. , 2017, Cell reports.

[6]  C. Hetz,et al.  Endoplasmic reticulum proteostasis impairment in aging , 2017, Aging cell.

[7]  R. Kaufman,et al.  ATF6 Decreases Myocardial Ischemia/Reperfusion Damage and Links ER Stress and Oxidative Stress Signaling Pathways in the Heart , 2017, Circulation research.

[8]  W. Paschen,et al.  Activation of the ATF6 branch of the unfolded protein response in neurons improves stroke outcome , 2017, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[9]  S. Houser,et al.  Acute Catecholamine Exposure Causes Reversible Myocyte Injury Without Cardiac Regeneration. , 2016, Circulation research.

[10]  Steven J Brown,et al.  Small molecule proteostasis regulators that reprogram the ER to reduce extracellular protein aggregation , 2016, eLife.

[11]  Vikas Kumar,et al.  Animal models of myocardial infarction: Mainstay in clinical translation. , 2016, Regulatory toxicology and pharmacology : RTP.

[12]  D. Yellon,et al.  Ischaemic conditioning and reperfusion injury , 2016, Nature Reviews Cardiology.

[13]  K. Margulies,et al.  Evidence for Intramyocardial Disruption of Lipid Metabolism and Increased Myocardial Ketone Utilization in Advanced Human Heart Failure , 2016, Circulation.

[14]  D. Yellon,et al.  Reducing myocardial infarct size: challenges and future opportunities , 2015, Heart.

[15]  N. Frangogiannis.  Pathophysiology of Myocardial Infarction. , 2015, Comprehensive Physiology.

[16]  Mark A Sussman,et al.  Hrd1 and ER-Associated Protein Degradation, ERAD, are Critical Elements of the Adaptive ER Stress Response in Cardiac Myocytes. , 2015, Circulation research.

[17]  R. Morimoto,et al.  The biology of proteostasis in aging and disease. , 2015, Annual review of biochemistry.

[18]  Kim Schneider,et al.  Preventing proteostasis diseases by selective inhibition of a phosphatase regulatory subunit , 2015, Science.

[19]  A. Nordheim,et al.  Rapid and highly efficient inducible cardiac gene knockout in adult mice using AAV-mediated expression of Cre recombinase. , 2014, Cardiovascular research.

[20]  Lisa M. Ryno,et al.  Unfolded protein response activation reduces secretion and extracellular aggregation of amyloidogenic immunoglobulin light chain , 2014, Proceedings of the National Academy of Sciences.

[21]  Herman I. May,et al.  Histone Deacetylase Inhibition Blunts Ischemia/Reperfusion Injury by Inducing Cardiomyocyte Autophagy , 2014, Circulation.

[22]  D. Mathis,et al.  Restoration of the Unfolded Protein Response in Pancreatic β Cells Protects Mice Against Type 1 Diabetes , 2013, Science Translational Medicine.

[23]  R. Hajjar,et al.  Targeting sarcoplasmic reticulum calcium ATPase by gene therapy. , 2013, Human gene therapy.

[24]  Jaykaran Charan,et al.  How to calculate sample size in animal studies? , 2013, Journal of pharmacology & pharmacotherapeutics.

[25]  Z. Dong,et al.  Mouse model of ischemic acute kidney injury: technical notes and tricks. , 2012, American journal of physiology. Renal physiology.

[26]  M. Lavail,et al.  Induction of endoplasmic reticulum stress genes, BiP and chop, in genetic and environmental models of retinal degeneration. , 2012, Investigative ophthalmology & visual science.

[27]  W. Chiang,et al.  Selective activation of ATF6 and PERK endoplasmic reticulum stress signaling pathways prevent mutant rhodopsin accumulation. , 2012, Investigative ophthalmology & visual science.

[28]  Peter J. Belmont,et al.  Protein disulfide isomerase-associated 6 is an ATF6-inducible ER stress response protein that protects cardiac myocytes from ischemia/reperfusion-mediated cell death. , 2012, Journal of molecular and cellular cardiology.

[29]  B. Aronow,et al.  A Thrombospondin-Dependent Pathway for a Protective ER Stress Response , 2012, Cell.

[30]  P. Walter,et al.  The Unfolded Protein Response: From Stress Pathway to Homeostatic Regulation , 2011, Science.

[31]  J. Weissman,et al.  Road to Ruin: Targeting Proteins for Degradation in the Endoplasmic Reticulum , 2011, Science.

[32]  C. Baines.  How and When Do Myocytes Die During Ischemia and Reperfusion: The Late Phase , 2011, Journal of cardiovascular pharmacology and therapeutics.

[33]  Andreas Bracher,et al.  Molecular chaperones in protein folding and proteostasis , 2011, Nature.

[34]  W. Balch,et al.  Modeling general proteostasis: proteome balance in health and disease. , 2011, Current opinion in cell biology.

[35]  F. Spinale,et al.  Pathophysiology of Myocardial Injury and Remodeling: Implications for Molecular Imaging , 2010, Journal of Nuclear Medicine.

[36]  E. Murphy,et al.  Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. , 2008, Physiological reviews.

[37]  R. Gottlieb,et al.  Localization of phosphorylated αB-crystallin to heart mitochondria during ischemia-reperfusion , 2008 .

[38]  R. Gottlieb,et al.  Localization of phosphorylated alphaB-crystallin to heart mitochondria during ischemia-reperfusion. , 2008, American journal of physiology. Heart and circulatory physiology.

[39]  D. Yellon,et al.  Myocardial reperfusion injury. , 2007, The New England journal of medicine.

[40]  R. Kaufman,et al.  ATF6alpha optimizes long-term endoplasmic reticulum function to protect cells from chronic stress. , 2007, Developmental cell.

[41]  P. Walter,et al.  Signal integration in the endoplasmic reticulum unfolded protein response , 2007, Nature Reviews Molecular Cell Biology.

[42]  D. Yellon,et al.  The evolving story of “conditioning” to protect against acute myocardial ischaemia–reperfusion injury , 2007, Heart.

[43]  C. Eckman,et al.  Regulation of Steady-state β-Amyloid Levels in the Brain by Neprilysin and Endothelin-converting Enzyme but Not Angiotensin-converting Enzyme* , 2006, Journal of Biological Chemistry.

[44]  Mark A Sussman,et al.  Endoplasmic Reticulum Stress Gene Induction and Protection From Ischemia/Reperfusion Injury in the Hearts of Transgenic Mice With a Tamoxifen-Regulated Form of ATF6 , 2006, Circulation research.

[45]  Jaw-Yuan Wang,et al.  以Sarco/Endoplasmic Reticulum Calcium ATPase 2表現作為大腸直腸癌的腫瘤標記 , 2006 .

[46]  H. Hoover,et al.  Sarco/endoplasmic Reticulum Calcium ATPase-2 Expression Is Regulated by ATF6 during the Endoplasmic Reticulum Stress Response , 2001, The Journal of Biological Chemistry.

[47]  L. Pitts,et al.  Rat middle cerebral artery occlusion: evaluation of the model and development of a neurologic examination. , 1986, Stroke.