Hi Levi, maybe oxidative stress + transcription factors...?

http://www.sciencedirect.com/science/article/pii/S000629520100836X (rat study though)

http://www.jneurosci.org/content/23/9/3597.short (neurons) 

http://www.sciencedirect.com/science/article/pii/S0300483X13000310 (expression of liver cells exposed to oxdants)

http://pubs.acs.org/doi/abs/10.1021/nl0507966 (expression of keratnocytes exposed to nanotubes)

i imagine Nrf2 will be in all of them, so that's a start i guess...

Thank you!  

Levi,

The following links (2015 articles) might help!

http://www.ncbi.nlm.nih.gov/pubmed/26122708?dopt=Abstract

Mechanisms of activation of the transcription factor Nrf2 by redox stressors, nutrient cues, and energy status and the pathways through which it attenuates degenerative disease.

http://www.sciencedirect.com/science/article/pii/S2213231715000701

Redox regulation of FoxO transcription factors

http://www.sciencedirect.com/science/article/pii/S2213231715000634

Regulation of Nox enzymes expression in vascular pathophysiology: Focusing on transcription factors and epigenetic mechanisms.

http://onlinelibrary.wiley.com/doi/10.1111/bph.13247/abstract

Eicosapentaenoic acid prevents TCDD-induced oxidative stress and inflammatory response by modulating MAP kinases and redox-sensitive transcription factors

Best...

Dear Levi Adams. We have published a paper in which HCV sub-genome replicon seems to  induce ROS and  stress signaling cascade and redox sensitive  AP1 transcription factor was activated. Please see below (Qadri et al., 2004 Biochem. J) Also attached is an abstract of  review article on HCV and ROS for some additional information and the review may be less relevant to your question

Biochem J. 2004 Mar 15;378(Pt 3):919-28.

Induced oxidative stress and activated expression of manganese superoxide dismutase during hepatitis C virus replication: role of JNK, p38 MAPK and AP-1.

Qadri I1, Iwahashi M, Capasso JM, Hopken MW, Flores S, Schaack J, Simon FR.

Activation of cellular kinases and transcription factors mediates the early phase of the cellular response to chemically or biologically induced stress. In the present study we investigated the oxidant/antioxidant balance in Huh-7 cells expressing the HCV (hepatitis C virus) subgenomic replicon, and observed a 5-fold increase in oxidative stress during HCV replication. We used MnSOD (manganese-superoxide dismutase) as an indicator of the cellular antioxidant response, and found that its activity, protein levels and promoter activity were significantly increased, whereas Cu/ZnSOD was not affected. The oxidative stress-induced protein kinases p38 MAPK (mitogen-activated protein kinase) and JNK (c-Jun N-terminal kinase) were activated in the HCV repliconcontaining cells and in Huh-7 cells transduced with Ad-NS5A [a recombinant adenovirus encoding NS5A (non-structural protein 5A)], coupled with a 4-5-fold increase in AP-1 (activator protein-1) DNA binding. Ava.1 cells, which encode a replication-defective HCV replicon, showed no significant changes in MnSOD, p38 MAPK or JNK activity. The AP-1 inhibitors dithiothreitol and N -acetylcysteine, as well as a dominant negative AP-1 mutant, significantly reduced AP-1 activation, demonstrating that this activation is oxidative stress-related. Exogenous NS5A had no effect on AP-1 activation in vitro, suggesting that NS5A acts at the upstream targets of AP-1 involving p38 MAPK and JNK signalling cascades. AP-1-dependent gene expression was increased in HCV subgenomic replicon-expressing Huh-7 cells. MnSOD activation was blocked by inhibitors of JNK (JNKI1) and p38 MAPK (SB203580), but not by an ERK (extracellular-signal-regulated kinase) inhibitor (U0126), in HCV-replicating and Ad-NS5A-transduced cells. Our results demonstrate that cellular responses to oxidative stress in HCV subgenomic replicon-expressing and Ad-NS5A-transduced cells are regulated by two distinct signalling pathways involving p38 MAPK and JNK via AP-1 that is linked to increased oxidative stress and therefore to an increased antioxidant MnSOD response.

PMID:  14670077  [PubMed - indexed for MEDLINE]  PMCID:  PMC1224028  Free PMC Article

Virol J. 2013 Aug 7;10:251. doi: 10.1186/1743-422X-10-251.

Oxidative stress and hepatitis C virus.

Paracha UZ1, Fatima K, Alqahtani M, Chaudhary A, Abuzenadah A, Damanhouri G, Qadri I.

Author information

Abstract

The disproportionate imbalance between the systemic manifestation of reactive oxygen species and body's ability to detoxify the reactive intermediates is referred to as oxidative stress. Several biological processes as well as infectious agents, physiological or environmental stress, and perturbed antioxidant response can promote oxidative stress. Oxidative stress usually happens when cells are exposed to more electrically charged reactive oxygen species (ROS) such as H2O2 or O2-. The cells' ability to handle such pro-oxidant species is impeded by viral infections particularly within liver that plays an important role in metabolism and detoxification of harmful substances. During liver diseases (such as hepatocellular or cholestatic problems), the produced ROS are involved in transcriptional activation of a large number of cytokines and growth factors, and continued production of ROS and Reactive Nitrogen Species (RNS) feed into the vicious cycle. Many human viruses like HCV are evolved to manipulate this delicate pro- and antioxidant balance; thus generating the sustainable oxidative stress that not only causes hepatic damage but also stimulates the processes to reduce treatment of damage. In this review article, the oxidant and antioxidant pathways that are perturbed by HCV genes are discussed. In the first line of risk, the pathways of lipid metabolism present a clear danger in accumulation of viral induced ROS. Viral infection leads to decrease in cellular concentrations of glutathione (GSH) resulting in oxidation of important components of cells such as proteins, DNA and lipids as well as double strand breakage of DNA. These disorders have the tendency to lead the cells toward cirrhosis and hepatocellular carcinoma in adults due to constant insult. We have highlighted the importance of such pathways and revealed differences in the extent of oxidative stress caused by HCV infection.

PMID:  23923986  [PubMed - indexed for MEDLINE]  PMCID:  PMC3751576

Thank you sir!

Hi Levi,

I'm not sure what the basis of your search is of course, but if it is from a molecular point of view these reviews might be interesting to you: 

This review by Claudia Cremers and Ursula Jacob is very informative: http://www.jbc.org/content/early/2013/07/16/jbc.R113.462929

If you're new to redox signalling and biochemistry, this perspective might be very useful to you as well (it might help to interpret many of the data out there): http://www.ncbi.nlm.nih.gov/pubmed/21459321

Also, we have recently written a review on disulphide-dependent signalling that includes some examples of (disulphide-mediated) redox signalling events that might be of interest: http://www.ncbi.nlm.nih.gov/pubmed/25109988 

Finally, this is quite a long one but there might be some leads in there for you: http://www.ncbi.nlm.nih.gov/pubmed/24634836

Best,

Marrit

You can check a paper I wrote

Free Radical Biology & Medicine, Vol. 27, Nos. 9/10, pp. 936 –944, 1999

Can be down loaded from my page

Andre Patrick Arrigo

See:

Biswas et al. Redox modification of protein thiols, emerging roles in cell signaling

Biochem Pharmacol 71, 2006, 551-564.

Chanda et al. triggering and modulation of apoptosis by oxidative stress Free Rad Biol Med 29, 2000, 323-333.

Filomeni et al. cell signalling and the glutathioner redox system. Biochem Pharmacol 64, 2002, 1057-1064.

Jabs et al. reactive oxygen intermediates as modulators of programmed cell death in plants and animals. Biochem Pharmacol 57, 1999, 231-245.

Jung et al. The Nrf2 system as a potential target for the development of indirect oxidants. Mplecules 15, 2010, 7266-7291.

Mates et al. intracellular redox status and oxidative stress: implication for cell proliferation, apoptosis and carcinogenesis. Arch Toxicol 82, 2008, 273-299.

Reddy et al. Genetic dissection of the Nfr2-dependent redox signaling-regulated transcriptional programs of cell proliferation and cytoprotection. Physiol genomics 32, 2007, 74-81.

Best regards

D Duval Ph.D.

You are right to question the validity of the findings reported in the literature. I have seen many papers in which researchers report using cells in room air (supraphysiologic) oxygen as their baseline and then try to induce more oxidative stress on top of that! Be careful to look for reports in which researchers use physiologically relevant oxygen conditions for cell incubation and handling, like this one:

http://www.ncbi.nlm.nih.gov/pubmed/26073944