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[DOI] [PMC free article] [PubMed] [Google Scholar] McTigue D.M., Tripathi R.B
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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
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