A gate-modulated nanowire oxide photosensor is fabricated by electron-beam lithography and conventional dry etch processing.. The device characteristics are good, including endurance of up to 10(6) test cycles, and gate-pulse excitation is used to remove persistent photoconductivity. The viability of nanowire oxide phototransistors for high speed and high resolution applications is demonstrated, thus potentially expanding the scope of exploitation of touch-free interactive displays.
Abstract-Vascular endothelial growth factor (VEGF) is a critical regulator of endothelial cell biology and vascular function. Chronic VEGF treatment has been shown to inhibit tumor necrosis factor-induced apoptosis in endothelial cells. However, the mechanism for this cell survival is unclear. Interestingly, VEGF also enhances the expression of X-linked inhibitor of apoptosis (XIAP), a well-established antiapoptotic factor. XIAP has been shown to suppress apoptosis by blocking caspase activity in cancer cells, but it remains under studied in the endothelium. Therefore, we hypothesized that VEGF affects important endothelial functions, such as apoptosis and cell migration, by regulating XIAP expression and downstream caspase activity. To test this hypothesis, caspase activity, apoptosis, and cell migration were assessed following XIAP overexpression or depletion in bovine aortic endothelial cells. Much like VEGF treatment, ectopic expression of XIAP blocked tumor necrosis factor-induced apoptosis. Surprisingly, the mechanism was caspase-independent. In addition, XIAP-associated cell survival was the result of enhanced nitric oxide (NO) production, and XIAP was partially localized in caveolae. In these lipid rafts, XIAP interacted with a regulator of NO production, caveolin-1, via a binding motif (FtFgtwiY, where the bold letters represent aromatic amino acids) in the baculoviral IAP repeat-3 domain. Endothelial NO synthase binding to caveolin-1 was competitively inhibited by XIAP, suggesting that XIAP acts as a modulator of NO production by releasing endothelial NO synthase from caveolin-1. Further studies showed that endothelial cell migration was also controlled by XIAP-dependent NO. Taken Key Words: VEGF Ⅲ XIAP Ⅲ caveolin-1 Ⅲ nitric oxide Ⅲ apoptosis E xtensive study of apoptosis has revealed a dichotomy of functions in the vascular system. In the endothelium, apoptosis contributes significantly to vascular pathology, as well as normal physiological function. In atherosclerotic plaques, apoptosis weakens the endothelial cell layer, promoting plaque rupture and atherothrombosis. 1 In contrast, apoptosis also acts as an important physiological mediator, eliminating unbalanced, harmful cells and maintaining vascular homeostasis. 2 Thus, the definition of apoptosis as an either physiological or pathological phenomenon requires careful dissection of distinct vascular apoptotic processes.Vascular endothelial growth factor (VEGF) is an endothelial cytokine that acts through the activation of VEGF receptor tyrosine kinases, eg, flkA/KDR and flt-1. 3 It is an important regulator of angiogenesis 4 and cell survival, or antiapoptosis, [5][6][7] and has been shown to act as a survival factor for newly formed blood vessels. Additional studies have found that VEGF also upregulates antiapoptotic proteins such as the inhibitors of apoptosis (IAPs) in human umbilical vein endothelial cells (HUVECs). 8 Cellular IAP homologs have been identified in many organisms, from yeasts to higher-order animals. 9 An important family m...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.