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glutathione reductase disulfide bridge The System: A Journey from Cyanobacteria to Higher Eukaryotes Model of electron flow in
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However, Bax-deficient animals, though protected initially from hepatocyte necrosis, succumbed to liver injury at later time points due to the sustained mitochondrial oxidant stress63, suggesting that in the absence of Bax, alternate mechanisms of mitochondrial protein release are activated in the face of sustained oxidant insult

Our results similarly indicate that GLP-1RAs increase ABCA1 and SR-B1 expression in PA-treated HepG2 cells, independent of LXR-mediated regulation of ABCA1

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