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Cardiolipin in the outer membrane also facilitates the transformation of multiple amyloidogenic proteins into pore-forming oligomers that can disrupt the membrane potential, leading to destruction of the mitochondrion, and, in the extreme case, initiation of an apoptotic cascade
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Table 1: Recent completion of the 1000 Genomes Project 13 has allowed us to update the estimation of the prevalence of G6PD deficiency (Fig 1)
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pGFP-Kif5c was a gift from M
