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Direct Targeting of Connexin-43 to Adherens Junctions and SK Channel Regulation of Granulocyte Reactive Oxygen Species Production

出版	University of California, San Francisco, 2006
ISBN	05427087289780542708725
URL	http://books.google.com.hk/books?id=yCnwdHELqN4C&hl=&source=gbs_api

註釋Membrane channels permit the movement of ions and small molecules across cell membranes, and are essential for electrical activity and solute homeostasis. Potassium channels are a class of ion channel that is selective for K+, and mediate the recovery phase of neuronal and cardiac action potentials, in addition to their roles in salt balance, volume regulation, calcium signaling, and apoptosis in non-excitable cells. Chapter 2 of this thesis explores the role of a small-conductance, calcium-actiavted K+ channel (SK) in reactive oxygen species (ROS) production by neutrophils, immune cells that use ROS and antimicrobial proteins to kill pathogenic microbes. This study shows that increasing SK activity in neutrophils and the neutrophil-like PLB-985 cell line enhances ROS formation by an NADPH-oxidase-independent pathway, and also increases PLB-985 apoptosis. A second study, in Chapter 3, focuses on the localization of gap junctions, clusters of connexin (Cx) proteins that span the membranes of adjacent cells and allow cells to exchange cytoplasmic small molecules. Deconvolution microscopy, imaging of live and fixed cells, and siRNA knockdown of the proteins beta-catenin, EB1, and p150(Glued) are used to probe the interactions between Cx-43, microtubule plus-ends, and the adherens junction. This work proposes a novel mechanism for gap junction protein delivery directly to cell-cell borders, mediated by the capture of microtubule plus-ends by adherens junction proteins. A third study finds that nuclei can co-localize to cell-cell borders with gap junctions, and shows by nuclear microinjection that gap junctions can mediate the exchange of small molecules between the nuclei of adjacent cells.