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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Jun and Fos regulation of NAD(P)H: quinone oxidoreductase gene expression.

NAD(P)H:Quinone oxidoreductase1 (NQO1) is a flavoprotein which promotes obligatory two-electron reduction of quinones, preventing their participation in redox cycling, oxidative stress and neoplasia. High levels of NQO1 have been observed in several kinds of tumours including that of the liver, lung, colon and breast. Transcription of the NQO1 gene is increased in response to bifunctional [e.g. beta-naphthoflavone (beta-NF), 2,3,7,8,-tetrachlordibenzo-p-dioxin (dioxin)] and monofunctional [phenolic antioxidants/chemoprotectors e.g. 2(3)tert-butyl-4-hydroxy-anisole (BHA)] inducers. High basal expression of the NQO1 gene and its induction by beta-NF and BHA are mediated by 31 bp of the antioxidant response element (ARE) containing more than one copy of the AP1/ AP1-like binding sites, Jun and Fos and other(s) as yet unknown regulatory proteins. The arrangement of AP1/ AP1-like elements within a short region of DNA may be important for beta-NF and BHA response. The high basal expression of the NQO1 gene in several types of tumour tissues may be due to a high expression and/or modification of regulatory proteins that result from tumour formation. Signal transduction from beta-NF and BHA for increased expression of the NQO1 gene involve metabolism of beta-NF and generation of 'redox signals'. The sequence of events after generation of 'redox signals' leading to the modification/activation of regulatory proteins that bind to ARE and increase expression of the NQO1 gene are less clear. The possibilities include involvement of protein(s) which receive signals from beta-NF and BHA and modulate the Jun and Fos proteins for increased binding to the ARE element or increased activities of the transcriptional activation domains of the regulatory proteins. The modifications in the regulatory proteins may be reduction of a cysteine residue in the DNA binding domain and/or phosphorylation of the DNA binding/transcriptional activation domains. Further studies are required to identify the intermediary components in the signal transduction pathway to completely understand the mechanism of induction of the NQO1 gene expression in response to beta-NF and BHA. Dioxin induction of the NQO1 gene expression is mediated by XRE, an element best characterized in the case of the CYP1A1 gene.(ABSTRACT TRUNCATED AT 400 WORDS)[1]


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