RAS signaling and prolonged interferon-beta stimulation promote generation of reactive oxygen species (ROS)

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Reaction [omitted]
Homo sapiens
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Oncogenic RAS signaling leads to mitochondrial dysfunction, resulting in increased mitochondrial production of reactive oxygen species (ROS), which contributes to cellular senescence (Moiseeva et al. 2009). The exact biochemical mechanism of RAS-induced mitochondrial dysfunction has not been established. Prolonged exposure to interferon-beta (INFB, INF-beta) also results in increased ROS concentration in the cell and triggers cellular senescence (Moiseeva et al. 2006). Although the positive regulation of ROS production by interferon signaling is well documented (Huang et al. 2007, Yang et al. 2007, Yim et al. 2012), the precise mechanism is not known.
Literature References
PubMed ID Title Journal Year
17765224 Pro-inflammatory cytokines increase reactive oxygen species through mitochondria and NADPH oxidase in cultured RPE cells

Petty, HR, Till, GO, Elner, SG, Yang, D, Bian, ZM, Elner, VM

Exp. Eye Res. 2007
22683641 The mitochondrial pathway and reactive oxygen species are critical contributors to interferon-?/?-mediated apoptosis in Ubp43-deficient hematopoietic cells

Kim, KI, Yang, Y, Yim, HY, Lim, JS, Zhang, DE, Lee, MS

Biochem. Biophys. Res. Commun. 2012
16826196 Coupling mitochondrial respiratory chain to cell death: an essential role of mitochondrial complex I in the interferon-beta and retinoic acid-induced cancer cell death

Huang, G, Cao, X, Lu, H, Chen, Y

Cell Death Differ. 2007
19528227 Mitochondrial dysfunction contributes to oncogene-induced senescence

Ferbeyre, G, DeschĂȘnes-Simard, X, Roux, A, Bourdeau, V, Moiseeva, O

Mol. Cell. Biol. 2009
16436515 DNA damage signaling and p53-dependent senescence after prolonged beta-interferon stimulation

Ferbeyre, G, Mallette, FA, Moores, A, Mukhopadhyay, UK, Moiseeva, O

Mol. Biol. Cell 2006
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