Erik A. Blackwood

ATF6 Decreases Myocardial Ischemia/Reperfusion Damage and Links ER Stress and Oxidative Stress Signaling Pathways in the Heart.

CaMKIIδ subtypes differentially regulate infarct formation following ex vivo myocardial ischemia/reperfusion through NF-κB and TNF-α.

Pharmacologic ATF6 activating compounds are metabolically activated to selectively modify endoplasmic reticulum proteins.

ATF6 Regulates Cardiac Hypertrophy by Transcriptional Induction of the mTORC1 Activator, Rheb.

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

Unfolding the Roles of Mitochondria as Therapeutic Targets for Heart Disease.

Integrating ER and Mitochondrial Proteostasis in the Healthy and Diseased Heart.

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.

The ER Unfolded Protein Response Effector, ATF6, Reduces Cardiac Fibrosis and Decreases Activation of Cardiac Fibroblasts.

Designing Novel Therapies to Mend Broken Hearts: ATF6 and Cardiac Proteostasis.

Reactive Oxygen Species (ROS)-Activatable Prodrug for Selective Activation of ATF6 after Ischemia/Reperfusion Injury.

ATF6 as a Nodal Regulator of Proteostasis in the Heart.

Mesencephalic astrocyte-derived neurotrophic factor is an ER-resident chaperone that protects against reductive stress in the heart.

Proteomic analysis of the cardiac myocyte secretome reveals extracellular protective functions for the ER stress response.