Stress activated transcription factors

The problem is that oxidative stress is a necessary part of our response to infection without it, we are unable to mount a genetic defence against pathogens. Oxidative stress activates transcription factors such as NFkB, which coordinate the broader genetic response promoting inflammation and stress resistance.5 Unfortunately, the rise in oxidative stress during ageing also activates NFkB. The pressure to eliminate infection in youth is... 

Brown SL, Sekhar KR, Rachakonda G, Sasi S, Freeman ML. 2008. Activating transcription factor 3 is a novel repressor of the nuclear factor erythroid-derived 2-related factor 2 (Nrf2)-regulated stress pathway. Cancer Res 68 364-368. 

Vanadium compounds are also believed to interact with cellular stress pathways that lead to apoptosis [70], as shown in Figure 11.3. One way vanadium compounds can influence these processes is by catalyzing the formation of intracellular ROS and NOS. All of the phosphorylation/dephosphorylation reactions eventually activate transcription factors that move to the nucleus to initiate the DNA breakdown characteristic of apoptosis. Vanadium is postulated to interfere with the dephosphorylation of some of these proteins by inhibition of various protein phosphatases. The... 

In in vivo and in vitro studies, Al can potentiate the oxidative stress produced by Fe [41, 42], Transcription factor, nuclear factor (NF)-fcB is activated by oxidative stress. The relevance of NF- cB to neurodegeneration is suggested by a correlation between the amount of activated transcription factor NF-/cB and a key inflammatory enzyme, COX-2, in both aging and AD temporal lobe neocortex [43],... 

DNA binding of AP-1 and NFkB is concentration-dependent and corresponds to Draize scores for ocular irritancy. Test chemical exposure time and probelabeling efficiency may introduce variance to results. Despite the variance, detection of altered expression and/or activation of stress-response transcription factors like AP-1 and NFkB can serve as an early marker for subsequent deteriorative outcomes (Ramesh et al. 1999) of ocular toxicity. 

Yoshida, H., Matsui, T, Yamamoto, A., Okada, T. and Mori, K. (2001) XBPl mRNAis induced by ATF6 and spliced by IREl in response to ER stress to produce a highly active transcription factor. Cell 107, 881-891. 

Nanoparticles in lungs at critical dose levels can initiate the oxidative stress-responsive transcription factors, such as nuclear factor kB (NFkB) and activator protein-1, and then translate the oxidative stress to release proinflammatory proteins such as IL6 and IL8 (64). This may lead to chronic degenerative pulmonary and cardiovascular disease. It is possible but not as yet proven that surface factors may trigger oxidative stress (64). 

FIGURE 12.1 Activation of PPARa by dietary oxidized lipids is mediated by binding of hydroxy or hydroperoxy fatty acids, such as 9-HODE, 13-HODE, and 13-HPODE contained in the oxidized lipids to the PPARa protein which subsequently forms a complex with RXR. The PPARa/RXR complex binds to specific DNA sequences, called PPRE, present in and around the promoter of PPAR target genes, and, thereby, stimulates their transcription. PPARa can also negatively regulate transcription of genes, which are under the control of stress-sensitive transcription factors such as NF-kB and encode proteins involved in the stress and inflammation response. This is the molecular basis for the well-documented antiinflammatory effects of PPARa. 

Varady, J., K. Eder, and R. Ringseis. 2011. Dietary oxidized fat activates the oxidative stress-responsive transcription factors NF-kB and Nrf2 in intestinal mucosa of mice. Euro em JoumglafNM j iQjl50 601-9. 

In mammals, there are three proximal sensors of BR stress that are localized to the BR membrane (a) protein kinase RNA (PKR)-like BR protein kinase (PBRK) (b) activating transcription factor 6 (ATF6) and (c) inositol-requiring enzyme 1 (ERBl) [149],... 

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