Inhibition of PTPs by H2O2 regulates the activation of distinct MAPK pathways

Cisplatin-induced apoptosis in human malignant testicular germ cell lines depends on MEK/ERK activation

“…In this respect, recent data support the hypothesis that toxic substances such as reactive oxygen species may inhibit phosphatases (e.g. protein phosphatase or protein tyrosine phosphatases) and thereby contribute to the activation of ERK (Lee and Esselman, 2002) Another scenario may be that CDDP ligates growth factor receptors, thereby activating the MEK -ERK pathway, as suggested for the cervical carcinoma cell line HeLa (Wang et al, 2000). Indeed there are even some reports demonstrating that TGCT express an aberrant platelet-derived growth factor areceptor, which is hypothetically capable of activating the MEK -ERK pathway upon ligation (Kollmannsberger et al, 2002;Palumbo et al, 2002).…”

Involvement of ROS and JNK1 in selenite-induced a poptosisin Chang liver cells

“…In addition, recent studies showed that ROS could activate the MAPKs. β-Amyloid caused the production of ROS and subsequent JNK activation (Jang and Surh, 2002), and ROS induced the phosphorylation of JNK, ERK and p38 kinases (Sano et al, 2001;Lee and Esselman, 2002). These results indicated that selenite induced intracellular ROS production, and consequential activation of JNK might play a role in apoptosis induction.…”

Profiling the NIH Small Molecule Repository for Compounds That Generate H2O2by Redox Cycling in Reducing Environments

“…[1][2][3][4]6,7 Several important classes of protein targets are susceptible to H 2 O 2 -mediated inactivation, including protein tyrosine phosphatases (PTPs), cysteine proteases (cathepsins and caspases), and metalloenzymes. [1][2][3][4][6][7][8][9][10][11][12][13][14] Redox cycling compounds (RCCs) generate H 2 O 2 in the presence of strong reducing agents such as DTT and tris(2-carboxyethyl)phosphine (TCEP), but not in the presence of weaker reducing agents like β-mercaptoethanol (BME), glutathione (GSH), or cysteine (Cys). 1,3,7 However, DTT and TCEP are commonly utilized in high-throughput screening (HTS) buffers to preserve the reduced state of critical amino acids and to maintain the catalytic activity or the folding of target proteins.…”