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Full-Text Articles in Life Sciences
Lipid Aldehydes Are Substrates And Transcriptional Regulators Of Cytochromes P450., Immaculate Amunom
Lipid Aldehydes Are Substrates And Transcriptional Regulators Of Cytochromes P450., Immaculate Amunom
Electronic Theses and Dissertations
4-hydroxy-2-nonenal (4-HNE) and propene-2-al (acrolein) are highly reactive á,â-unsaturated aldehydes. 4-HNE and acrolein are generated in vivo as products of lipid peroxidation. These aldehydes are implicated in the onset of several diseases including atherosclerosis and neurodegenerative disease. They also react with nucleophilic cellular macromolecules including proteins, DNA and phospholipids. Some of these reactions in vivo lead to inhibition of enzyme activities, depletion of glutathione and oxidative stress. Because of their pathophysiological relevance, attention has focused during the last decade on the ability of mammals to metabolize these lipid aldehydes. The purpose of this study was therefore to determine the role …
Mitochondria In Energy-Limited States: Mechanisms That Blunt The Signaling Of Cell Death, Steven C. Hand, Michael A. Menze
Mitochondria In Energy-Limited States: Mechanisms That Blunt The Signaling Of Cell Death, Steven C. Hand, Michael A. Menze
Michael Menze
Cellular conditions experienced during energy-limited states – elevated calcium, shifts in cellular adenylate status, compromised mitochondrial membrane potential – are precisely those that trigger, at least in mammals, the mitochondrion to initiate opening of the permeability transition pore, to assemble additional protein release channels, and to release pro-apoptotic factors. These proapototic factors in turn activate initiator and executer caspases. How is activation of mitochondria-based pathways for the signaling of apoptotic and necrotic cell death avoided under conditions of hypoxia, anoxia, diapause, estivation and anhydrobiosis? Functional trade-offs in environmental tolerance may have occurred in parallel with the evolution of diversified pathways …
Mitochondria In Energy-Limited States : Mechanisms That Blunt The Signaling Of Cell Death., Steven Hand, Michael Menze
Mitochondria In Energy-Limited States : Mechanisms That Blunt The Signaling Of Cell Death., Steven Hand, Michael Menze
Faculty Scholarship
Cellular conditions experienced during energy-limited states – elevated calcium, shifts in cellular adenylate status, compromised mitochondrial membrane potential – are precisely those that trigger, at least in mammals, the mitochondrion to initiate opening of the permeability transition pore, to assemble additional protein release channels, and to release pro-apoptotic factors. These proapototic factors in turn activate initiator and executer caspases. How is activation of mitochondria-based pathways for the signaling of apoptotic and necrotic cell death avoided under conditions of hypoxia, anoxia, diapause, estivation and anhydrobiosis? Functional trade-offs in environmental tolerance may have occurred in parallel with the evolution of diversified pathways …