SIRT1 contributes to aldose reductase expression through modulating NFAT5 under osmotic stress: In vitro and in silico insights
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- 作者：Ahmet Can Timucin cantimucin@sabanciuniv.edu" class="auth_mail" title="E-mail the corresponding author ; Cagri Bodur cagribodur@gmail.com" class="auth_mail" title="E-mail the corresponding author ; Huveyda Basaga ; huveyda@sabanciuniv.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：AK ; acetyllysine ; AP-1 ; activator protein 1 ; AR ; aldose reductase ; BGT1 ; betaine/gamma-aminobutyric acid transporter ; Egr-1 ; early growth response protein 1 ; FSP27 ; fat-specific protein 27 ; HSP90 ; heat shock protein 90 ; NAD+ ; nicotinamide adenine dinucleotide ; NADPH ; nicotinamide adenine dinucleotide phosphate ; NFAT5 ; nuclear factor of activated T-cells 5 ; ORE ; osmotic response element ; p38 ; mitogen-activated protein kinase p38 ; p53 ; cellular tumor antigen p53 ; p65 ; transcription factor p65 ; PAR
- 刊名：Cellular Signalling
- 出版年：2015
- 出版时间：November 2015
- 年：2015
- 卷：27
- 期：11
- 页码：2160-2172
- 全文大小：1926 K
文摘
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An osmotic stress model was generated via 16 h of 100 mM NaCl in U937 cells.
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Expression of AR and NFAT5 was regulated by SIRT1 modulators in this model.
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Modulation of AR and NFAT5 by SIRT1 was validated in HeLa cells.
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SIRT1 activity increased binding of NFAT5 to AR ORE region.
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SIRT1 directly targets at least one lysine, K282 of NFAT5, in silico.