Effect of phenol inducing antioxidant responsive element on D. melanogaster lifespan

2012 ◽  
Vol 2 (3) ◽  
pp. 221-229 ◽  
Author(s):  
N. Ya. Weisman ◽  
E. B. Men’shchikova ◽  
N. K. Zenkov ◽  
N. V. Kandalintseva ◽  
M. D. Golubovsky
Keyword(s):  
Responsive Element ◽  
Antioxidant Responsive Element

Sulforaphane Induces Thioredoxin through the Antioxidant-Responsive Element and Attenuates Retinal Light Damage in Mice

2005 ◽  
Vol 46 (3) ◽  
pp. 979 ◽  
Author(s):  
Masaki Tanito ◽  
Hiroshi Masutani ◽  
Yong-Chul Kim ◽  
Mai Nishikawa ◽  
Akihiro Ohira ◽  
...  
Keyword(s):  
Light Damage ◽  
Retinal Light Damage ◽  
Responsive Element ◽  
Antioxidant Responsive Element

Nrf2, not the estrogen receptor, mediates catechol estrogen-induced activation of the antioxidant responsive element

2003 ◽  
Vol 1629 (1-3) ◽  
pp. 92-101 ◽  
Author(s):  
Jong-Min Lee ◽  
Peter C. Anderson ◽  
Janette K. Padgitt ◽  
Janean M. Hanson ◽  
Christopher M. Waters ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Catechol Estrogen ◽  
Responsive Element ◽  
Antioxidant Responsive Element

scholarly journals Role of the Tumor Suppressor PTEN in Antioxidant Responsive Element-mediated Transcription and Associated Histone Modifications

2009 ◽  
Vol 20 (6) ◽  
pp. 1606-1617 ◽  
Author(s):  
Kensuke Sakamoto ◽  
Kenta Iwasaki ◽  
Hiroyuki Sugiyama ◽  
Yoshiaki Tsuji
Keyword(s):  
Tumor Suppressor ◽  
Jurkat Cells ◽  
Nuclear Accumulation ◽  
Human Leukemia ◽  
Creb Binding Protein ◽  
Cell Functions ◽  
The Status ◽  
Responsive Element ◽  
Ferritin H ◽  
Antioxidant Responsive Element

Coordinated regulation of PI3-kinase (PI3K) and the tumor suppressor phosphatase and tensin homologue deleted on chromosome 10 (PTEN) plays a pivotal role in various cell functions. PTEN is deficient in many cancer cells, including Jurkat human leukemia. Here, we demonstrate that the status of PTEN determines cellular susceptibility to oxidative stress through antioxidant-responsive element (ARE)-mediated transcription of detoxification genes. We found that ferritin H transcription was robustly induced in tert-butylhydroquinone (t-BHQ)-treated Jurkat cells via an ARE, and it was due to PTEN deficiency. Chromatin immunoprecipitation assays revealed that p300/CREB-binding protein (CBP) histone acetyltransferases and Nrf2 recruitment to the ARE and Bach1 release were blocked by the PI3K inhibitor LY294002, along with the partial inhibition of Nrf2 nuclear accumulation. Furthermore, acetylations of histone H3 Lys9 and Lys18, and deacetylation of Lys14 were associated with the PI3K-dependent ARE activation. Consistently, PTEN restoration in Jurkat cells inhibited t-BHQ–mediated expression of ferritin H and another ARE-regulated gene NAD(P)H:quinone oxidoreductase 1. Conversely, PTEN knockdown in K562 cells enhanced the response to t-BHQ. The PTEN status under t-BHQ treatment affected hydrogen peroxide-mediated caspase-3 cleavage. The PI3K-dependent ferritin H induction was observed by treatment with other ARE-activating agents ethoxyquin and hemin. Collectively, the status of PTEN determines chromatin modifications leading to ARE activation.

scholarly journals Nuclear Factor-E2-related Factor-1 Mediates Ascorbic Acid Induction of Osterix Expression via Interaction with Antioxidant-Responsive Element in Bone Cells

2007 ◽  
Vol 282 (30) ◽  
pp. 22052-22061 ◽  
Author(s):  
Weirong Xing ◽  
Anny Singgih ◽  
Anil Kapoor ◽  
Catrina M. Alarcon ◽  
David J. Baylink ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Bone Cells ◽  
Related Factor ◽  
Nuclear Factor ◽  
Responsive Element ◽  
Antioxidant Responsive Element
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