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Tommaso Galeotti

Researcher at The Catholic University of America

Publications -  101
Citations -  4525

Tommaso Galeotti is an academic researcher from The Catholic University of America. The author has contributed to research in topics: Superoxide dismutase & Lipid peroxidation. The author has an hindex of 37, co-authored 100 publications receiving 4325 citations. Previous affiliations of Tommaso Galeotti include Catholic University of the Sacred Heart.

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Reactive oxygen species as essential mediators of cell adhesion: the oxidative inhibition of a FAK tyrosine phosphatase is required for cell adhesion.

TL;DR: Evidence is provided that intracellular ROS are generated after integrin engagement and that these oxidant intermediates are necessary for integrin signaling during fibroblast adhesion and spreading and a synergistic action of integrins and RTKs for redox signaling is proposed.
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Reactive Oxygen Species as Downstream Mediators of Angiogenic Signaling by Vascular Endothelial Growth Factor Receptor-2/KDR

TL;DR: In this paper, the involvement of reactive oxygen species (ROS) in the mitogenic cascade initiated by the tyrosine kinase receptors of several growth factor peptides was investigated.
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Metastasis: cancer cell’s escape from oxidative stress

TL;DR: It is suggested that metastasis represents an integrated strategy for cancer cells to avoid oxidative damage and escape excess ROS in the primary tumor site, explaning why redox signaling pathways are often up-regulated in malignancy and metastasis.
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Oxidative stress and antioxidant defenses in ethanol-induced cell injury.

TL;DR: The consistent induction of the mitochondrial antioxidant enzyme manganese superoxide dismutase (Mn-SOD) observed in experimental animals after acute and chronic ethanol administration has all the characteristics of a "stress response" to an oxidative insult.
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A redox signaling mechanism for density-dependent inhibition of cell growth.

TL;DR: The arrest of growth induced by cell confluence is shown to be due, at least in part, to a decrease in the steady-state levels of intracellular ROS and the consequent impairment of mitogenic redox signaling.