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Cerebellar Degeneration In Harlequin Mice Is Associated With Inflammation Unaltered By Low-Dose Phenobarbital Treatment, Anita Prtenjaca
Cerebellar Degeneration In Harlequin Mice Is Associated With Inflammation Unaltered By Low-Dose Phenobarbital Treatment, Anita Prtenjaca
Electronic Thesis and Dissertation Repository
Canadian population demographics are shifting to an increase in aged individuals and an increase in the prevalence of neurodegenerative diseases. The post-mitotic nature of most neurons highlights the need to understand the etiology and early mechanisms in neurodegenerative diseases and design targeted therapies. Currently, the etiologies of neurodegeneration are poorly understood but oxidative stress, mitochondrial dysfunction and inflammation are early mechanisms in Alzheimer’s disease, Parkinson’s disease and Amyotrophic Lateral Sclerosis. An anti-aging strategy that can be adapted for use in neurodegeneration is hormesis, where repeated low-level exposures to stressors are beneficial to the cell. Hormesis has demonstrated efficacy in inhibiting …
Substrate And Regulation Of Mitochondrial Μ-Calpain, Aashish Joshi
Substrate And Regulation Of Mitochondrial Μ-Calpain, Aashish Joshi
University of Kentucky Doctoral Dissertations
μ -Calpain is localized to the mitochondrial intermembrane space. Apoptosisinducing factor (AIF), which executes caspase-independent cell death, is also localized to the mitochondrial intermembrane space. Following processing at the N-terminus, AIF becomes truncated (tAIF) and is released from mitochondria. The protease responsible for AIF processing has not been established. The same submitochondrial localization of mitochondrial μ-calpain and AIF gives support to the hypothesis that mitochondrial μ-calpain may be responsible for processing AIF. Atractyloside-induced tAIF release in rat liver mitochondria was inhibited by cysteine protease inhibitor MDL28170, but not by calpain inhibitors PD150606 or calpastatin. Moreover, μ-calpain immunoreactivity was difficult to …