FUNDED STUDIES

Researchers

FUNDED STUDIES

Researchers

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Researcher

J. Cesar Cardenas earned his Ph.D. from the University of Chile, where he studied the mechanism that regulated nuclear Ca2+ under Dr. Enrique Jaimovich’s mentoring. Then he moved to the University of Pennsylvania Medical School where he explored the nuclear localization 1,4,5-trisphosphate receptor (InsP3R) Ca2+channel by using high resolution electron microscopy and cryofracture as a postdoctoral fellow with Dr. Clara Franzini-Armstrong. Motivate in gain a better understanding of the physiological role of the InsP3R he joined Dr. Kevin Foskett’s lab also at UPENN, where he developed a strong interest in the regulation of cellular metabolism and bioenergetics by Ca2+. He was the first to show that basal constitutive low-level Ca2+ signaling by the InsP3R, is essential to maintain the sufficient mitochondrial NADH production to support oxidative phosphorylation in resting cells. In the absence of this calcium signaling, cells become metabolically compromised and a pro-survival AMPK-dependent mTOR-independent autophagy is turned on. He joined the Department of Anatomy and Cell Developmental Biology Program at the Institute of Biomedical Science of the University of Chile School of Medicine in March of 2012.

Researcher’s Projects

Researcher

J. Cesar Cardenas PhD., Universidad Mayor, Santiago, Chile

J. Cesar Cardenas earned his Ph.D. from the University of Chile, where he studied the mechanism that regulated nuclear Ca2+ under Dr. Enrique Jaimovich’s mentoring. Then he moved to the University of Pennsylvania Medical School where he explored the nuclear localization 1,4,5-trisphosphate receptor (InsP3R) Ca2+channel by using high resolution electron microscopy and cryofracture as a postdoctoral fellow with Dr. Clara Franzini-Armstrong. Motivate in gain a better understanding of the physiological role of the InsP3R he joined Dr. Kevin Foskett’s lab also at UPENN, where he developed a strong interest in the regulation of cellular metabolism and bioenergetics by Ca2+. He was the first to show that basal constitutive low-level Ca2+ signaling by the InsP3R, is essential to maintain the sufficient mitochondrial NADH production to support oxidative phosphorylation in resting cells. In the absence of this calcium signaling, cells become metabolically compromised and a pro-survival AMPK-dependent mTOR-independent autophagy is turned on. He joined the Department of Anatomy and Cell Developmental Biology Program at the Institute of Biomedical Science of the University of Chile School of Medicine in March of 2012.

Researcher’s Projects

Active Research Projects
Active Clinical Projects
Past Projects
Active Research Projects
Active Clinical Projects
Past Projects