Christopher C. Glembotski

A role for the p38 mitogen-activated protein kinase pathway in myocardial cell growth, sarcomeric organization, and cardiac-specific gene expression.

Coordination of ATF6-mediated transcription and ATF6 degradation by a domain that is shared with the viral transcription factor, VP16.

Expression and functional characterization of SCaMPER: a sphingolipid-modulated calcium channel of cardiomyocytes.

Mimicking phosphorylation of alphaB-crystallin on serine-59 is necessary and sufficient to provide maximal protection of cardiac myocytes from apoptosis.

Factor associated with neutral sphingomyelinase activation and its role in cardiac cell death.

Opposing roles for ATF6alpha and ATF6beta in endoplasmic reticulum stress response gene induction.

Overexpression of mitogen-activated protein kinase kinase 6 in the heart improves functional recovery from ischemia in vitro and protects against myocardial infarction in vivo.

Atrial natriuretic peptide promotes cardiomyocyte survival by cGMP-dependent nuclear accumulation of zyxin and Akt.

Endoplasmic reticulum stress gene induction and protection from ischemia/reperfusion injury in the hearts of transgenic mice with a tamoxifen-regulated form of ATF6.

Activation of the unfolded protein response in infarcted mouse heart and hypoxic cultured cardiac myocytes.

Effects of the isoform-specific characteristics of ATF6 alpha and ATF6 beta on endoplasmic reticulum stress response gene expression and cell viability.

Getting a G--RRP on regulated exocytosis in the heart.

Endoplasmic reticulum stress in the heart.

Pim-1 regulates cardiomyocyte survival downstream of Akt.

The role of the unfolded protein response in the heart.

Coordination of growth and endoplasmic reticulum stress signaling by regulator of calcineurin 1 (RCAN1), a novel ATF6-inducible gene.

Mesencephalic astrocyte-derived neurotrophic factor is an ischemia-inducible secreted endoplasmic reticulum stress response protein in the heart.

LPS-induced autophagy is mediated by oxidative signaling in cardiomyocytes and is associated with cytoprotection.

Ischemia activates the ATF6 branch of the endoplasmic reticulum stress response.

The ATF6-Met[67]Val substitution is associated with increased plasma cholesterol levels.

Roles for endoplasmic reticulum-associated degradation and the novel endoplasmic reticulum stress response gene Derlin-3 in the ischemic heart.

Pim-1 kinase protects mitochondrial integrity in cardiomyocytes.

Functions for the cardiomyokine, MANF, in cardioprotection, hypertrophy and heart failure.

The cardiokine story unfolds: ischemic stress-induced protein secretion in the heart.

Regulation of microRNA expression in the heart by the ATF6 branch of the ER stress response.

Protein disulfide isomerase-associated 6 is an ATF6-inducible ER stress response protein that protects cardiac myocytes from ischemia/reperfusion-mediated cell death.

Mesencephalic astrocyte-derived neurotrophic factor protects the heart from ischemic damage and is selectively secreted upon sarco/endoplasmic reticulum calcium depletion.

Limitation of individual folding resources in the ER leads to outcomes distinct from the unfolded protein response.

Clarifying the cardiac proteasome paradox: protein quality control.

New concepts of endoplasmic reticulum function in the heart: programmed to conserve.

Roles for the sarco-/endoplasmic reticulum in cardiac myocyte contraction, protein synthesis, and protein quality control.

ATF6 [corrected] and thrombospondin 4: the dynamic duo of the adaptive endoplasmic reticulum stress response.

Regulation of cardiac hypertrophic signaling by prolyl isomerase Pin1.

Pathological hypertrophy amelioration by PRAS40-mediated inhibition of mTORC1.

Mechanistic target of rapamycin complex 2 protects the heart from ischemic damage.

Roles for ATF6 and the sarco/endoplasmic reticulum protein quality control system in the heart.

Classic studies of cultured cardiac myocyte hypertrophy: interview with a transformer.

Finding the missing link between the unfolded protein response and O-GlcNAcylation in the heart.

Hrd1 and ER-Associated Protein Degradation, ERAD, are Critical Elements of the Adaptive ER Stress Response in Cardiac Myocytes.

Breaking down the COP9 Signalsome in the heart: how inactivating a protein ubiquitin ligase increases protein ubiquitylation and protects the heart.

Activation of the ATF6 branch of the unfolded protein response in neurons improves stroke outcome.

S100A4 protects the myocardium against ischemic stress.

Junctophilin-2 gene therapy rescues heart failure by normalizing RyR2-mediated Ca release.

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.

Expanding the Paracrine Hypothesis of Stem Cell-Mediated Repair in the Heart: When the Unconventional Becomes Conventional.

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.

Proteostasis and Beyond: ATF6 in Ischemic Disease.

Physiological signaling in the absence of amidated peptides.

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.