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Kai Chen

Researcher at University of Connecticut

Publications -  57
Citations -  4486

Kai Chen is an academic researcher from University of Connecticut. The author has contributed to research in topics: Medicine & Oxidative stress. The author has an hindex of 28, co-authored 45 publications receiving 4131 citations. Previous affiliations of Kai Chen include Boston Medical Center & Boston University.

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Regulation of ROS signal transduction by NADPH oxidase 4 localization

TL;DR: It is demonstrated that nicotinamide adenine dinucleotide phosphate reduced oxidase 4 (Nox4), a major Nox isoform expressed in nonphagocytic cells, including vascular endothelium, is localized to the endoplasmic reticulum (ER), indicating that the specificity of intracellular ROS-mediated signal transduction may be modulated by the localization of Noxisoforms within specific subcellular compartments.
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Altered Mitochondrial Dynamics Contributes to Endothelial Dysfunction in Diabetes Mellitus

TL;DR: Findings implicate increased mitochondrial fission as a contributing mechanism for endothelial dysfunction in diabetic states through increased reactive oxygen species production.
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Hydrogen peroxide activates endothelial nitric-oxide synthase through coordinated phosphorylation and dephosphorylation via a phosphoinositide 3-kinase-dependent signaling pathway.

TL;DR: Data indicate that H2O2 promotes calcium-dependent eNOS activity through a coordinated change in the phosphorylation status of the enzyme mediated by Src- and ErbB receptor-dependent PI 3-K activation.
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Neurons Overexpressing Heme Oxygenase‐1 Resist Oxidative Stress‐Mediated Cell Death

TL;DR: It is suggested that induction of HO‐1 by pharmacological means may be a novel approach to amelioration of oxidative insults to neurons.
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A role for malonyl-CoA in glucose-stimulated insulin secretion from clonal pancreatic beta-cells.

TL;DR: The data are consistent with a metabolic model in which malonyl-CoA mediates the switch from fatty acid catabolism to lipid synthesis during glucose stimulation of beta-cells, and it is suggested that these changes in lipid metabolism could play a pivotal role in the regulation of the sustained phase of insulin secretion.