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GPX1 — NFKB1

Pathways - manually collected, often from reviews:

• WikiPathways Oxidative Stress: NFKB1/SP1/NFE2L2 → HMOX1/GPX1/GPX3/NQO1/UGT1A6 (activation)
  

Text-mined interactions from Literome

Zhou et al., Free Radic Biol Med 2001 : To test whether NF kappa B or AP-1 might be mediating the induction of GPx and CAT in muscle cells subjected to oxidative stress, we first characterized their activation by pro-oxidants ... In summary, our results suggest that NF kappa B and AP-1 are important mediators of redox-responsive gene expression in skeletal muscle, and that at least NF kappa B is actively involved in the upregulation of the GPx and CAT in response to oxidative stress
Fan et al., J Biol Chem 2003 (Anoxia) : Overexpression of glutathione peroxidase-1 or catalase, but not Mn-SOD or Cu, Zn-SOD, significantly reduced both NF kappa B activation and tyrosine phosphorylation of I kappa B alpha
Lei et al., Annu Rev Nutr 2007 (Chronic Disease) : Intracellular and tissue levels of GPX1 activity affect apoptotic signaling pathway, protein kinase phosphorylation, and oxidant mediated activation of NFkappaB
Viña et al., Biol Chem 2008 : Activation of NF-kappa B by estrogens subsequently activates the expression of Mn-SOD and GPx , but genistein is only capable of activating Mn-SOD expression
Kretz-Remy et al., J Cell Biol 1996 : Inhibition of I kappa B-alpha phosphorylation and degradation and subsequent NF-kappa B activation by glutathione peroxidase overexpression