147 results on '"Blackwood, Erik A."'
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2. Abstract 17132: IRE1α Protects Against Cardiac Fibrosis via Regulating Selective Transcript Degradation
3. Abstract 15535: SGK1 is a Key Mediator of Pathological Cardiac Fibrosis
4. Modeling heart failure with preserved ejection fraction in female mice: an elusive target
5. Design and Production of Heart Chamber-Specific AAV9 Vectors
6. CaMKII delta subtypes differentially regulate infarct formation following ex vivo myocardial ischemia/reperfusion through NF-kappa B and TNF-alpha
7. CaMKIIδ subtypes differentially regulate infarct formation following ex vivo myocardial ischemia/reperfusion through NF-κB and TNF-α.
8. Abstract 11876: The Selenoprotein, Vimp, Selectively Regulates a Newly Defined Non-Canonical Form of Proteasomal Degradation at the ER to Modulate Cardiac Hypertrophy
9. Proteomic analysis of the cardiac myocyte secretome reveals extracellular protective functions for the ER stress response
10. ER-Specific Autophagy or ER-Phagy in Cardiac Myocytes Protects the Heart Against Doxorubicin-Induced Cardiotoxicity
11. Roles for ATF6-Inducible Genes in Cardiac Physiology and Pathology
12. CaMKIIδ subtypes differentially regulate infarct formation following ex vivo myocardial ischemia/reperfusion through NF-κB and TNF-α
13. Abstract 15063: The Atf6-inducible Selenoprotein, Vimp, Regulates Proteostasis and Pressure Overload-induced Heart Failure
14. Optimization of Large‐Scale Adeno‐Associated Virus (AAV) Production
15. ATF6 Regulates Cardiac Hypertrophy by Transcriptional Induction of the mTORC1 Activator, Rheb
16. Pharmacologic ATF6 activation confers global protection in widespread disease models by reprograming cellular proteostasis
17. Dietary choline intake is necessary to prevent systems‐wide organ pathology and reduce Alzheimer's disease hallmarks
18. Noncanonical Form of ERAD Regulates Cardiac Hypertrophy
19. Exploration of chamber-specific promoters and miRNAs for the generation of chamber-specific AAV9 technology
20. The selenoprotein, VIMP, exacerbates cardiac pathology by selectively impeding a newly defined non-canonical ERAD in the heart
21. Dietary choline intake is necessary to prevent systems-wide organ pathology and reduce Alzheimer’s disease hallmarks
22. Abstract 21206: Manf, a Structurally Unique Redox-Sensitive Chaperone, Restores ER-Protein Folding in the Ischemic Heart
23. Abstract 20269: The Stress Response Transcription Factor ATF6 is Necessary for Compensatory Cardiac Hypertrophy
24. Abstract 19559: Effect of Isoforms of ATF6 in Cardiac Myocytes
25. Abstract 19303: A Small Molecular Activator of the ER Proteostasis Regulator, ATF6, is Beneficial in the Ischemic Heart
26. Abstract 19298: Age-related Decline of the Adaptive Proteostasis Gene Program in Cardiac Myocytes
27. ATF6 Decreases Myocardial Ischemia/Reperfusion Damage and Links ER Stress and Oxidative Stress Signaling Pathways in the Heart
28. Hydrogen sulfide: the gas that fuels longevity
29. Abstract 14305: Diastolic Dysfunction and Activation of Ventricular and Atrial Unfolded Protein Response in a Novel Gottingen Miniswine Model of Heart Failure With Preserved Ejection Fraction
30. Age-related decline of the unfolded protein response in the heart promotes protein misfolding and cardiac pathology
31. Optimizing Adeno-Associated Virus Serotype 9 for Studies of Cardiac Chamber–Specific Gene Regulation
32. The peroxisomal enzyme, FAR1, is induced during ER stress in an ATF6-dependent manner in cardiac myocytes
33. Mesencephalic astrocyte–derived neurotrophic factor is an ER‐resident chaperone that protects against reductive stress in the heart
34. Simultaneous Isolation and Culture of Atrial Myocytes, Ventricular Myocytes, and Non-Myocytes from an Adult Mouse Heart
35. Mesencephalic astrocyte–derived neurotrophic factor is an ER-resident chaperone that protects against reductive stress in the heart
36. ATF6 as a Nodal Regulator of Proteostasis in the Heart
37. ATF6β is an Adaptive Transcription Factor in Cardiac Myocyte.
38. Small Nppa and Myl2 Promoters Are Sufficient to Maintain Chamber‐specific Expression on an AAV9 Platform
39. Designing Novel Therapies to Mend Broken Hearts: ATF6 and Cardiac Proteostasis
40. The ER Unfolded Protein Response Effector, ATF6, Reduces Cardiac Fibrosis and Decreases Activation of Cardiac Fibroblasts
41. Sledgehammer to Scalpel: Broad Challenges to the Heart and Other Tissues Yield Specific Cellular Responses via Transcriptional Regulation of the ER-Stress Master Regulator ATF6α
42. Integrating ER and Mitochondrial Proteostasis in the Healthy and Diseased Heart
43. Reactive Oxygen Species (ROS)-Activatable Prodrug for Selective Activation of ATF6 after Ischemia/Reperfusion Injury
44. Abstract 260: The ER Unfolded Protein Response Effector, ATF6, Reduces Fibrosis and Moderates Activation of Cardiac Fibroblasts
45. Unfolding the Roles of Mitochondria as Therapeutic Targets for Heart Disease
46. Abstract 17305: The ER Unfolded Protein Response Effector, ATF6, Promotes Proliferation and Maintains Pluripotency in Cardiac Stem Cells
47. Pharmacologic ATF6 Activation Confers Global Protection in Widespread Disease Models by Reprogramming Cellular Proteostasis
48. Pharmacologic ATF6 activating compounds are metabolically activated to selectively modify endoplasmic reticulum proteins
49. Abstract 352: Manf, a Structurally Unique Redox-sensitive Chaperone, Restores Er-protein Folding in the Ischemic Heart
50. Abstract 479: The ER Unfolded Protein Response Effector, ATF6, Promotes Proliferation and Maintains Pluripotency in Cardiac Stem Cells
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