Role of redox potential and reactive oxygen species in stress signaling

This review summarizes the current understanding of the mechanisms contributing to reactive oxygen species -related changes in key stress activated signaling cascades

Victor Adler; Zhimin Yin; Kenneth D Tew; Ze'ev Ronai


Scholarcy highlights

  • Homeostatic control of reactive oxygen species is one of the key determinants in maintaining cell growth pathways which can incorporate proliferation apoptosis and senescence
  • Examples given in this review clearly suggest that ROS effects on cellular stress response involve almost all cellular compartments and regulatory levels
  • Our current knowledge points to the existence of ROS-related feedback loops, which ensure that the changes elicited upon ROS formation will be homeostatic and cyclical
  • Given the complexity of ROS regulating enzyme/systems, one could envision additional regulatory circuits that could increase the degree of sensitivity and responsiveness
  • Glutathione depletion has been implicated in the regulation of stress kinases JNK and p38, inactivation of PKC and attenuated Bcl2 inhibition of apoptotic protease which induces DNA fragmentation, the nature of these changes is not completely understood
  • Broad-spectrum protein phosphatase inhibitors decreased UTP incorporation
  • Since tumor cells are often found to express elevated levels of ROS responsive proteins and different drug resistance and apoptotic capacity, it is suggested that altering ROS control may sensitize tumor cells for a better response to selective treatments
  • While the dimerized form of thioredoxin dissociates from respective kinases, within the nuclei it has been shown to associate with the glucocorticoid receptor, which increases Glucocorticoid receptors transcriptional activities

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