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Zoltan Arany

Researcher at University of Pennsylvania

Publications -  155
Citations -  15370

Zoltan Arany is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 48, co-authored 110 publications receiving 12878 citations. Previous affiliations of Zoltan Arany include Cardiovascular Institute of the South & Harvard University.

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Activation of Hypoxia-inducible Transcription Factor Depends Primarily upon Redox-sensitive Stabilization of Its α Subunit

TL;DR: Results suggest that an intact redox-dependent signaling pathway is required for destablization of the HIF-1α protein, which was rapidly and drastically decreased in vivo following an abrupt increase to normal oxygen tension.
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HIF-independent regulation of VEGF and angiogenesis by the transcriptional coactivator PGC-1α

TL;DR: PGC-1α and ERR-α, major regulators of mitochondrial function in response to exercise and other stimuli, also control a novel angiogenic pathway that delivers needed oxygen and substrates, and may provide a novel therapeutic target for treating ischaemic diseases.
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PGC-1α protects skeletal muscle from atrophy by suppressing FoxO3 action and atrophy-specific gene transcription

TL;DR: The high levels of P GC-1α in dark and exercising muscles can explain their resistance to atrophy, and the rapid fall in PGC-1 α during atrophy should enhance the FoxO-dependent loss of muscle mass.
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An essential role for p300/CBP in the cellular response to hypoxia

TL;DR: In this article, the intact cDNA for HIF-1α and p300/CBP were cloned and shown to participate in the induction of hypoxia-responsive genes, including vascular endothelial growth factor.
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Transcriptional coactivator PGC-1α controls the energy state and contractile function of cardiac muscle

TL;DR: Using genetic knockout mice, it is shown that, while PGC-1alpha KO mice appear to retain normal mitochondrial volume in both muscle beds, expression of genes of oxidative phosphorylation is markedly blunted, indicating that P GC-1 alpha is vital for the heart to meet increased demands for ATP and work in response to physiological stimuli.