Regulation under the Impact of RNI

OxyR Fur LAC9 Acel —rather uniform results showing activation -de-repression of genes that are under the control of Fur —attenuated DNA-binding in vitro —inhibition of DNA-binding in yeast 

NF-kB AP-1 Spl, Egr-1 (zinc finger TFs) VDR, RXR (nuclear hormone R) PPARy NFAT HSFs p53 HIF-1 -activation in resting cells, low level RNI -inhibition in stimulated cells, high level RNI -activation in unstimulated cells, low level RNI -inhibition in activated cells -rather uniform inhibition -activation if Spl de-represses the e.g. TNFa promoter -inhibition of DNA-binding and reporter activity -activation at low level RNI -inhibition at high level RN I —inhibition in activated N K cells -activation (HSP70 expression) —activation (for details see below) -activation under normoxia (for details see below) -inhibition under hypoxia 

TF transcription factor, R receptor, Fur ferric uptake regulation protein, NF-kB nuclear factor-kB, AP-1 activator protein-1, Egr-1 early growth response-1, VDR la,25-dihydroxy-vitamin D3 receptor, RXR retinoid X receptor, PPARy peroxisome proliferator-activated receptor y NFAT nuclear factor of activated T-cells, HSF heat shock factor, p53 tumor suppressor p53, HIF-1 hypoxia inducible factor-1.  

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Numerous studies have analyzed the regulatory effects of RNI on transcription factors and transcriptional regulation. Although outside the main focus of this article, to summarize these primary observations we provide a table showing several transcription factors and their regulation under the impact of RNI (Table 13.1). For extensive coverage of the primary literature we refer to a number of review articles [11-14],... 

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