Abstract
Nrf2 controls the basal expression of genes regulated through the antioxidant responsive element (ARF). It also contributes to the inducible expression of certain members of the ARE-gene battery. Under normal dietary conditions, the expression of class Alpha and class Mu glutathione S-transferase (GST) isoenzymes and NAD(P)H:quinone oxidoreductase (NQO) in the liver and small intestine is reduced significantly in nrf 2 (-/-) mice. Administration of chemopreventive agents to wildtype mice can result in marked induction of hepatic and intestinal GST and NQO. However, the extent of induction of these detoxication enzymes in the nrf 2 knockout mouse is variable, suggesting gene-specific effects.
| Original language | English |
|---|---|
| Pages (from-to) | 291-294 |
| Number of pages | 4 |
| Journal | Chemico-Biological Interactions |
| Volume | 133 |
| Issue number | 1-3 |
| Publication status | Published - 2001 Feb 28 |
Keywords
- Cancer chemoprevention
- Glutathione S-transferase
- NAD(P)H: quinone oxidoreductase
- Nrf2
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In: Chemico-Biological Interactions, Vol. 133, No. 1-3, 28.02.2001, p. 291-294.
Research output: Contribution to journal › Article › peer-review
TY - JOUR
T1 - The Nrf2 transcription factor regulates basal expression of class alpha and class Mu glutathione S-transferases in the mouse, but not necessarily their induction by cancer chemopreventive agents
AU - McMaghon, Michale
AU - Chanas, Simon A.
AU - Henderson, Colin J.
AU - Wolf, C. Roland
AU - Yamamoto, Masayuki
AU - Hayes, John D.
N1 - Funding Information: Support for the research has been obtained from the Swedish Research Council for Engineering Sciences, the Swedish Natural Science Research Council, the Swedish Cancer Society, and the Carl Trygger Foundation. Funding Information: This work was supported by an Australian Research Council Project Grant and an Australian Research Council Senior Research Fellowship (to M.W.P.), a National Health and Medical Research Council Postgraduate Research Scholarship and an International Centre for Diffraction Data Crystallography Scholarship (to A.J.O.), an Australian Research Council Postdoctoral Fellowship (to J.R.) and a National Research Council of Italy Grant (to G.R. and M.L.B.). Funding Information: The author would like to acknowledge the invaluable contributions by the postgraduate students and staff of the Protein Structure-Function Research Programme and Richard Armstrong (Vanderbilt University) to this work. Financial support was provided by Wits University, National Research Foundation, Alexander von Humboldt Foundation and FIRCA(NIH) grant TW00779. Funding Information: A.-M. Abdalla was supported by a scholarship from the Egyptian Government. This work was funded by grants from the Swedish Natural Science Research Council and the Carl Trygger Foundation for Scientific Research. Funding Information: In part supported by grants GM32304 (YCA), CA77495 (SA), VA Merit Review (PZ), and CA55589 (SVS). Funding Information: This work was funded by Aventis Crop Science UK Ltd. Funding Information: The authors would like to acknowledge Jim Parsons, Gaoyi Xioa, and Marcia Newcomer for their assistance with various aspects of this project. Monetary support from the NIH and the Training Program in Molecular Biophysics is also acknowledged. Funding Information: We thank the staff of ESRF synchrotron, Grenoble and the SRS synchrotron, Daresbury for help with data collection. Financial support from ESRF for our visit to Grenoble is gratefully acknowledged. We also acknowledge Aventis Crop Science UK Ltd. for funding this project. Funding Information: I gratefully acknowledge Jim Parsons at the Vanderbilt University School of Medicine for the generation of the recombinant mutant plasmids. This work was supported by the University of the Witwatersrand, the South African National Research Foundation, the Fogarty International Collaboration Award TW00779, Grant GM30910 from the National Institutes of Health and the Alexander von Humboldt Foundation. Funding Information: This work was supported by the University of the Witwatersrand, the South African National Research Foundation and the Fogarty International Research Collaboration Award TW00779. Funding Information: The Andrew Mellon Foundation, the University of the Witwatersrand and the South African National Research Foundation for financial support. Funding Information: Funding for this project was provided by grants from the National Institutes of Health (R01-EOS9427) and the U.S. Environmental Protection Agency (R 827441)– Funding Information: The Finnish studies were supported by the Academy of Finland, the Finnish Konkordia Foundation, and EVO funds from Kuopio University Hospital. The French study was supported by the Swiss Cancer League, the League against Cancer of Fribourg, the Cancer Research (Switzerland) and the Gustave–Roussy Institute (France). Funding Information: H.J.L. was supported by NIH grants 1R01CA66782 and 1R01CA73403. Funding Information: The research in our laboratory is supported by grants from The Swedish Medical Research Council and from AstraZeneca. Funding Information: We thank the Cancer Research Campaign, British Medical Association and British Lung Foundation for support. Funding Information: Supported by The North Staffordshire Medical Institute and the McCall Foundation. Funding Information: Financial support is acknowledged with grateful thanks from the International Programs in Chemical Sciences (IPICS), Uppsala University and the Research Board, University of Zimbabwe. Funding Information: Supported by the British Lung Foundation, MURST, Ministero del Lavoro e della Previdenza Sociale, Danish Research Academy and North Staffordshire Medical Institute. Funding Information: The work presented here was partially supported by the Deutsche Forschungsge-meinschaft (SFB 475). Funding Information: The author wishes to acknowledge the following collaborators, Richard N. Armstrong, Bryan Bernat and Richard Svensson in the kinetic studies and Hans Hebert in structural aspects. The studies were supported by the Swedish Cancer Society, The National Board for Laboratory Animals, Carl Tryggers Foundation and funds from Karolinska Insitutet. Funding Information: This work is supported by National Institute of Health Grants AI22531, AI31599, AR36308, ES06105, HL03208. Funding Information: Support from the Swedish Medical Research Council (projects no 31X-12573), the Swedish Society of Medicine, the Swedish Cancer Society, Harald Jeansson’s and Harald and Greta Jeansson’s, and the Karolinska Institutet foundations are gratefully acknowledged. Funding Information: This study was supported by the Swedish Cancer Society, The National Board for Laboratory Animals, Carl Tryggers Foundation and funds from Karolinska Institutet. Funding Information: This work was supported by United States Public Health Service Grants CA-66561 and T32-GM-08550. Funding Information: This study is part of special projects supported by Italian Ministry of University and of Scientific and Technological Research, Italian National Research Council and Italian Ministry of Health. Funding Information: The authors would like to acknowledge invaluable contributions of L.T. Laugh-lin, B. Bernat and Professor John Helman (Cornell University) to various aspects of this work. NIH Grants A142756 and GM30910 and the Training Program in Molecular Biophysics at Vanderbilt provided support for this work. Funding Information: This work was supported by grant CA-42448 from the National Institutes of Health. Funding Information: The author would like to thank Ralph Hermanns for technical assistance and Professor Peter van Bladeren for the rat GST isoenzymes. This research was funded by the Dutch Cancer Society (project RUL017-1407). Funding Information: This work was supported by the Swedish Natural Science Research Council and the Swedish Cancer Society. Funding Information: This work was supported in part by a grant from the Ministero dell’ Università e della Ricerca Scientifica e Tecnologica. Funding Information: This study was supported by the Swedish Cancer Society, The National Board for Laboratory Animals, Carl Tryggers Foundation and funds from Karolinska Insitutet. Funding Information: This work was supported in part by an Australian Research Council Project Grant and an Australian Research Council Senior Research Fellowship (to M.W. Parker), a National Research Council of Italy Grant (Target Project on Biotechnology, to G. Ricci), a National Health and Medical Research Council Postgraduate Research Scholarship and an International Centre for Diffraction Data Crystallography Scholarship (to A.J. Oakley) and an Australian Research Council Postdoctoral Fellowship (to J. Rossjohn). Funding Information: This work was supported by a grant from the National Science Foundation (MCB-9723308). Funding Information: This research was supported in part by National Institute of Environmental Health Sciences grant ES03127 to M.W.A. Funding Information: In part supported by grants CA27967 (YCA), CA77495 (SA), and ES07804 (PZ). Funding Information: This work was supported in part by NIH:NIEHS grant ES07804 (to PZ) and by a pilot grant from the University of Arkansas for Medical Science. Funding Information: This work was supported by the grant PRIN1998 n. 9805539127 from the MURST. Funding Information: This work was supported by grants from the U.S. National Cancer Institute (76420), the Howard Hughes Medical Institute, and the Oakland University Research Excellence Fund. Funding Information: This investigation received financial support from the UNDP:WORLD BANK: WHO Special Programme for Research and Training in Tropical Medicine (TDR0096 and TDR 980281). Funding Information: This work was supported in part by NIH:NIEHS grant ES07804 (to PZ). Funding Information: The ATPase activity of recombinant RalBP1 was only marginally stimulated by DNP-SG (by approximately 30%). This may indicate that the protein, as isolated from the bacterial lysate, is saturated with a tightly bound ligand and already near-maximally stimulated. Antibiotics used for plasmid selection are possible candidates for such ligands. This interpretation was supported by the fact that omitting chloramphenicol from the bacterial growth medium improved stimulation. Funding Information: This work was supported in part by VA Merit Review funding (to P. Zimniak) and NIH grants GM32304 (to Y.C. Awasthi) and CA77495 (to S. Awasthi). Funding Information: This work was supported in part by grant from the Ministero dell’ Università e della Ricerca Scientifica e Tecnologica. Funding Information: This work was supported in part by SNF grant 3100-050602.97 to S.V. Funding Information: This work is supported by the DFG (grant Li 1-3, 1-4). Funding Information: This work was funded by a grant from the Association of International Cancer Research (99-041, awarded to JDH and MY). Simon A. Chanas thanks the MRC and Zeneca for a collaborative Ph.D. studentship. Funding Information: This work was supported by the Research Science Funds of Serbia, Grant c03E18. Funding Information: This work was supported by MURST-40%; grants telethon-E872, AIRC, EU (QRLT-1999-00739); Ministero Sanità. Funding Information: This project was funded by the Norwegian Research Council. We thank Sigbjorn Andersen, Norwegian Institute of Water Research, for assistance with the fish exposure experiments. Funding Information: We thank Pedro Miguel Santos for sending pPR9TT plasmid and E. coli strains used in this work and P. Di Nardo for checking the English. This work was supported in part by European Community contract no. QLK3-CT1999–00041. Funding Information: This work was supported by a grant from the US Army Medical Research and Material Command (Breast Cancer Research Program). Funding Information: This work was supported by grants from the Swedish Natural Science Research Council and the Swedish Research Council for Engineering Sciences.We thank Marianne Ridderström and Gun Stenberg of our laboratory for valuable discussions.
PY - 2001/2/28
Y1 - 2001/2/28
N2 - Nrf2 controls the basal expression of genes regulated through the antioxidant responsive element (ARF). It also contributes to the inducible expression of certain members of the ARE-gene battery. Under normal dietary conditions, the expression of class Alpha and class Mu glutathione S-transferase (GST) isoenzymes and NAD(P)H:quinone oxidoreductase (NQO) in the liver and small intestine is reduced significantly in nrf 2 (-/-) mice. Administration of chemopreventive agents to wildtype mice can result in marked induction of hepatic and intestinal GST and NQO. However, the extent of induction of these detoxication enzymes in the nrf 2 knockout mouse is variable, suggesting gene-specific effects.
AB - Nrf2 controls the basal expression of genes regulated through the antioxidant responsive element (ARF). It also contributes to the inducible expression of certain members of the ARE-gene battery. Under normal dietary conditions, the expression of class Alpha and class Mu glutathione S-transferase (GST) isoenzymes and NAD(P)H:quinone oxidoreductase (NQO) in the liver and small intestine is reduced significantly in nrf 2 (-/-) mice. Administration of chemopreventive agents to wildtype mice can result in marked induction of hepatic and intestinal GST and NQO. However, the extent of induction of these detoxication enzymes in the nrf 2 knockout mouse is variable, suggesting gene-specific effects.
KW - Cancer chemoprevention
KW - Glutathione S-transferase
KW - NAD(P)H: quinone oxidoreductase
KW - Nrf2
UR - http://www.scopus.com/inward/record.url?scp=0003144095&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0003144095&partnerID=8YFLogxK
M3 - Article
AN - SCOPUS:0003144095
SN - 0009-2797
VL - 133
SP - 291
EP - 294
JO - Chemico-Biological Interactions
JF - Chemico-Biological Interactions
IS - 1-3
ER -