2006
DOI: 10.1096/fj.05-4376com
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Abstract: We have proposed that the age-associated increase of reactive oxygen species (ROS) by electron transport chain (ETC) dysfunction may cause the elevated basal level of p38 MAPK stress response pathway activity. However, the mechanism by which ROS activates this pathway is not clear. Here we propose that activation of the p38 MAPK pathway by complex I (CI) generated ROS, in response to rotenone (ROT) treatment, is based on the ability of reduced Trx to bind to and inhibit ASK 1 and its release from the complex u… Show more

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Cited by 180 publications
(191 citation statements)
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“…We did not observe an increase in chondrocyte JNK phosphorylation in response to menadione-induced oxidative stress but rather found increased phosphorylation of MMK-3/6 and p38 along with inhibition of IGF-1-mediated Akt activation. This was consistent with previous studies demonstrating that PRX and thioredoxin can act as negative regulators of cell death pathways by direct inhibition of the ASK1-MKK3/6-p38 pathway in mice (49) and cell lines (50), an effect inhibited by oxidative stress. ROS-induced inhibition of Akt was also found to result in activation of the ASK1-MKK3/6-p38 pathway, which caused cell death in several cell lines (51).…”
Section: Discussionsupporting
confidence: 93%
“…We did not observe an increase in chondrocyte JNK phosphorylation in response to menadione-induced oxidative stress but rather found increased phosphorylation of MMK-3/6 and p38 along with inhibition of IGF-1-mediated Akt activation. This was consistent with previous studies demonstrating that PRX and thioredoxin can act as negative regulators of cell death pathways by direct inhibition of the ASK1-MKK3/6-p38 pathway in mice (49) and cell lines (50), an effect inhibited by oxidative stress. ROS-induced inhibition of Akt was also found to result in activation of the ASK1-MKK3/6-p38 pathway, which caused cell death in several cell lines (51).…”
Section: Discussionsupporting
confidence: 93%
“…The MAPK family includes the extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK. They are activated in response to ischemiareperfusion-induced brain injury, and it is believed that the [27][28][29] . It should be noted that JNK and p38 are activated by proinflammatory cytokines and promote apoptosis [30] .…”
Section: Discussionmentioning
confidence: 99%
“…The ASK1-thioredoxin complex formation was shown to be regulated by ROS, which in turn determines ASK1 activity leading to ROSinduced apoptosis (Hsieh and Papaconstantinou, 2006). Therefore, antioxidant thioredoxin and antiapoptotic SOCS1 may regulate the apoptosis-inducing kinase system by a coordinated mechanism.…”
Section: Discussionmentioning
confidence: 99%