Proteomic analysis of the cardiac myocyte secretome reveals extracellular protective functions for the ER stress response.
Mesencephalic astrocyte-derived neurotrophic factor is an ER-resident chaperone that protects against reductive stress in the heart.
ATF6 Regulates Cardiac Hypertrophy by Transcriptional Induction of the mTORC1 Activator, Rheb.
ATF6 Decreases Myocardial Ischemia/Reperfusion Damage and Links ER Stress and Oxidative Stress Signaling Pathways in the Heart.
Junctophilin-2 gene therapy rescues heart failure by normalizing RyR2-mediated Ca(2+) release.
S100A4 protects the myocardium against ischemic stress.
Hrd1 and ER-Associated Protein Degradation, ERAD, are Critical Elements of the Adaptive ER Stress Response in Cardiac Myocytes.
PRAS40 prevents development of diabetic cardiomyopathy and improves hepatic insulin sensitivity in obesity.
Mechanistic target of rapamycin complex 2 protects the heart from ischemic damage.
Pathological hypertrophy amelioration by PRAS40-mediated inhibition of mTORC1.
Regulation of cardiac hypertrophic signaling by prolyl isomerase Pin1.
New concepts of endoplasmic reticulum function in the heart: programmed to conserve.
ATF6 [corrected] and thrombospondin 4: the dynamic duo of the adaptive endoplasmic reticulum stress response.
Limitation of individual folding resources in the ER leads to outcomes distinct from the unfolded protein response.
Mesencephalic astrocyte-derived neurotrophic factor protects the heart from ischemic damage and is selectively secreted upon sarco/endoplasmic reticulum calcium depletion.
The cardiokine story unfolds: ischemic stress-induced protein secretion in the heart.
Ischemia activates the ATF6 branch of the endoplasmic reticulum stress response.