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2008 Jan 24 [cited 2025 Apr 19];358(4):e4

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While the immediate consequence of amplification of mitochondrial oxidant stress is loss of mitochondrial protein function due to modification of thiols [33], peroxynitrite mediated nitrotyrosine formation [48] and oxidative mitochondrial DNA damage [41], the critical event resulting in escalation of cell wide damage is induction of the mitochondrial permeability transition (MPT)

This protein operates by exporting Gln in exchange for other amino acids, meeting the heightened demand for protein synthesis in cells and forming the basis for the proliferation of KRAS-mutant cells