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Nevertheless, experimental data suggest that the altered intracellular redox status associated with hyperhomo-cysteinemia-induced oxidant stress is the major molecular mechanism responsible for the atherothrombogenicity of moderately elevated circulating homocysteine
neoformans growth at elevated temperature, including Ras1 and Cdc42 signaling [157], the unfolded protein response [158], the histone acetyltransferase Gcn5 [159], the cell wall integrity pathway [160], and calcineurin signaling [19]
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Br J Clin Pharmacol 34:7981 Mitchell SJ, Hilmer SN, Murnion BP, Matthews S (2011) Hepatotoxicity of therapeutic short-course paracetamol in hospital inpatients: impact of ageing and frailty
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