K
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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Journal ArticleDOI
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.
Journal ArticleDOI
Altered Mitochondrial Dynamics Contributes to Endothelial Dysfunction in Diabetes Mellitus
Sherene M. Shenouda,Michael E. Widlansky,Kai Chen,Guoquan Xu,Monika Holbrook,Corey E. Tabit,Naomi M. Hamburg,Alissa A. Frame,Tara L. Caiano,Matthew A. Kluge,Mai-Ann Duess,Aaron Levit,Brian H Kim,Mor-Li Hartman,Lija Joseph,Orian S. Shirihai,Joseph A. Vita +16 more
TL;DR: Findings implicate increased mitochondrial fission as a contributing mechanism for endothelial dysfunction in diabetic states through increased reactive oxygen species production.
Journal ArticleDOI
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.
Journal ArticleDOI
A role for malonyl-CoA in glucose-stimulated insulin secretion from clonal pancreatic beta-cells.
Barbara E. Corkey,Major C. Glennon,Kai Chen,Jude T. Deeney,Franz M. Matschinsky,Marc Prentki +5 more
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.