The change in the nuclear redox environment induced by DEM could activate a shift in the activity of transcription factors that modulate cell cycle as we have demonstrated here with the decreased expression of Id2 in DEM treated cells.
It modulates cell responses to redox changes associated with the generation of reactive oxygen species, regulates apoptotic cell death, and mediates transmembrane transport of organic solutes.
The blue square marks proteins involved in cell redox homeostasis.
These promote chilling tolerance by maintaining cell redox homeostasis.
The results show that extracellular thiol/disulfide redox state modulates cell proliferation rate and that this control interacts with growth factor signaling apparently independently of cellular glutathione.
ROS can influence vascular, renal, and cardiac function and structure by modulating cell growth, contraction/dilatation, and inflammatory responses via redox-dependent signaling pathways.
ROS may trigger apoptosis via multiple mechanisms, of which the MAPK pathways are well-documented redox-sensitive mediators involved in modulating cell apoptosis.
The balance between the mitochondrial antioxidant detoxification system and ROS should be finely maintained while low levels mitochondrial ROS in are required by cells to modulate normal redox signaling networks.
We therefore hypothesized that anti-cancer therapies may modulate the redox state of cancer cell exofacial thiols.
Superoxide dismutase (SOD) is a class of enzymes that catalyze the dismutation of superoxide into oxygen and hydrogen peroxide [ 6], and modulate the redox status of eukaryotic cells.
