Oxidative stress-induced apoptosis is mediated by ERK1/2 phosphorylation

Oxidation-induced intramolecular disulfide bond inactivates mitogen-activated protein kinase kinase 6 by inhibiting ATP binding

“…Although our data here clearly show that oxidation inactivates MAP2Ks, paradoxically, some reports showed that oxidation could activate various MAPKs (29,36), whereas others claimed that oxidation had minimal effect on the activity of selected MAPKs (37,38). A survey of the literature suggests that the factors contributing to the confusion include different types and doses of oxidants, different cell types, as well as different treatment time used in various studies.…”

N-(4-Hydroxyphenyl)retinamide-induced apoptosis triggered by reactive oxygen species is mediated by activation of MAPKs in head and neck squamous carcinoma cells

“…ERK activation downstream of ROS has been shown to be mediated by different signaling pathways, including growth factor receptors (epidermal growth factor receptor, platelet-derived growth factor receptor), Ras and PKC (Guyton et al, 1996;Aikawa et al, 1997;Martindale and Holbrook, 2002;Lee et al, 2003). We observed that the pan-PKC inhibitor GF109203X suppressed ERK and p38 activation and apoptosis induced by 4HPR, suggesting that PKC may be an upstream regulator of ERK in our system.…”

“…Furthermore, oxidative stress has been shown to activate ERK as a protective mechanism (Guyton et al, 1996;Aikawa et al, 1997;Bhatt et al, 2002). However, a proapoptotic role has been demonstrated for ERK in several studies with different stimuli, including anticancer drugs (Stanciu et al, 2000;Wang et al, 2000;Guise et al, 2001;Xiao and Singh, 2002;Lee et al, 2003;Zhang et al, 2003;Nguyen et al, 2004).…”

Compensatory activation of ERK1/2 inAtg5-deficient mouse embryo fibroblasts suppresses oxidative stress-induced cell death

“…15 On the contrary, high levels of ROS can oxidize cell constituents, such as lipids, proteins and DNA, and thus induces cell death. [16][17][18] Various defense mechanisms have been developed to protect cells against oxidative stress, such as upregulation of anti-oxidants, removal of specific proteins by the ubiquitin-proteasome system, and removal of damaged proteins and organelles by autophagy. 19 Recently, oxidative stress-induced cell death is emphasized with autophagy.…”