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Taken together, these findings suggest that APR-246 could induce tumor cell death through both reactivation of mutant p53 and inhibition of cellular thiol-dependent redox system proteins (GPX4, TXNDR1, GRX1), providing novel combinatorial strategies for AML therapy
10.1111/j.1468-1331.2011.03414.x Eur
During AKI, mitochondria frequently exhibit morphological abnormalities, including swelling and fragmentation, which can facilitate the release of pro-apoptotic mediators and trigger the opening of the mitochondrial permeability transition pore
Mnh thy da khng qu cng n hi v em ny thin dng trng hn, lng m cha nn nh thoa kem dng tt nh
M.et al (2012)
Mesenchymal Stem/Stromal cell-Targeted Therapies for Solid Tumors and Hematological Malignancies
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