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Christopher C Glembotski
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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 Ca2+ 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
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