Redox-sensitive gene

Ganji, S.H., Qin, S., Zhang, L., Kamanna, V.S., and Kashyap, M.L., 2009. Niacin inhibits vascular oxidative stress, redox-sensitive genes, and monocyte adhesion to human aortic endothelial cells. Atherosclerosis. 202 68-75. 

The transcription of nir and nor genes in P. stutzeri (Cuypers and Zumft, 1992, 1993) and P. aeruginosa (Zimmermann et al., 1991) would appear to be controlled in part by homologs of the Fnr protein of E. coli (Guest, 1992) which is a redox sensitive, transcriptional activator. Fnr boxes (binding sequences) are located upstream from norC, nirM and nirS. It is likely therefore that Fnr-like proteins participate in a regulatory mechanism which derepresses the synthesis... 

It now seems that an overdose of paracetamol causes a massive chemical stress, which causes an immediate adaptive defense response in the liver cell, which senses danger via redox-sensitive transcription factors. A number of mechanisms are involved, including the release, as a result of the stress, of a transcription factor Nrf-2 from its binding with Keap 1, a cytoplasmic inhibitor. Nrf-2 translocates to the nucleus and with other activators binds to an antioxidant-response element. This leads to transcription of a number of genes, so producing a... 

Moreover GSH concentration indirectly controls a host of redox-sensitive transcription factors such as NF-kB and AP-1, modulates the genes for pro-inflammatory mediators as well as protective antioxidant genes such as y-GCS, Mn-superoxide dismutase, and heme oxygenase-1. Also TNF-a, p38 MAP kinase activation and p38 MAP kinase-mediated RANTES (regulated upon activation, normal T-cells expressed and secreted ) production is redox regulated [24]. The role of RANTES in the inflammatory and allergic response has been recently elucidated [25], indicating a role of intracellular GSH also in this particular field of inflammation. 

Marui et al. clarified the relation between oxidative stress in the arterial wall (in particular, the endothelium) and the development of the inflammatory response [19,25]. Expression of VCAM-1 by hmnan endothelial cells stimulated by cytokines such as interleukin-1 (IL-1) is mediated by redox-sensitive control mechanisms [25]. The redox-sensitive nature of this gene regulation was determined by the use of antioxidants that are active intracellularly. It was reported that the antioxidant pyrolidine dithiocarbamate (PDTC) inhibited the IL-1-induced endothelial expression of mRNA for VCAM-1 and was as effective as a monoclonal antibody against the VCAM-1 counterligand very late antigen-4 (VLA-4) in inhibiting binding of Molt-4 cells, which express VLA-4 [25]. 

In E. coli catalases are up-regulated by the redox-sensitive oxyR protein, which in its oxidized state binds to AREs, while up-regulation of SODs involves soxR and soxS gene products [69]. 

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