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

scholarly journals PIAS3 Interacts with ATF1 and Regulates the Human Ferritin H Gene through an Antioxidant-responsive Element

2007 ◽  
Vol 282 (31) ◽  
pp. 22335-22343 ◽  
Author(s):  
Kenta Iwasaki ◽  
Kiros Hailemariam ◽  
Yoshiaki Tsuji
Keyword(s):  
H Gene ◽  
Human Ferritin ◽  
Responsive Element ◽  
Ferritin H ◽  
Antioxidant Responsive Element

Susceptibility to Retinal Light Damage in Transgenic Rats with Rhodopsin Mutations

2003 ◽  
Vol 44 (2) ◽  
pp. 486 ◽  
Author(s):  
Daniel T. Organisciak ◽  
Ruth M. Darrow ◽  
Linda Barsalou ◽  
R. Krishnan Kutty ◽  
Barbara Wiggert
Keyword(s):  
Light Damage ◽  
Transgenic Rats ◽  
Retinal Light Damage ◽  
Rhodopsin Mutations

Evidence of Retinal Light Damage in Rana cascadae: A Declining Amphibian Species

Copeia ◽  
1998 ◽  
Vol 1998 (4) ◽  
pp. 906 ◽  
Author(s):  
Katherine V. Fite ◽  
Andrew Blaustein ◽  
Lynn Bengston ◽  
Heather E. Hewitt
Keyword(s):  
Light Damage ◽  
Amphibian Species ◽  
Retinal Light Damage ◽  
Rana Cascadae

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

The role of ocular pigmentation in protecting against retinal light damage

1980 ◽  
Vol 20 (12) ◽  
pp. 1127-1131 ◽  
Author(s):  
L.M. Rapp ◽  
T.P. Williams
Keyword(s):  
Light Damage ◽  
Retinal Light Damage

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.

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