Do Cysteine Residues Regulate Transient Receptor Potential Canonical Type 6 Channel Protein Expression?

被引:4
|
作者
Thilo, Florian [1 ]
Liu, Ying [2 ,3 ,4 ]
Krueger, Katharina [1 ]
Foerste, Nora [1 ]
Wittstock, Antje [1 ]
Scholze, Alexandra [2 ,3 ]
Tepel, Martin [1 ,2 ,3 ]
机构
[1] Charite Campus Benjamin Franklin, Dept Med, Div Nephrol, D-14195 Berlin, Germany
[2] Odense Univ Hosp, Dept Nephrol, DK-5000 Odense, Denmark
[3] Univ So Denmark, Inst Mol Med Cardiovasc & Renal Res, Inst Clin Res, Odense, Denmark
[4] Tenth Peoples Hosp Tongji Univ, Dept Urol, Shanghai, Peoples R China
关键词
N-ACETYLCYSTEINE; CELL-DEATH; HOMOCYSTEINE;
D O I
10.1089/ars.2011.4343
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The regulation of calcium influx through transient receptor potential canonical type 6 (TRPC6) channel is mandatory for the activity of human monocytes. We submit the first evidence that cysteine residues of homocysteine (HC) or acetylcysteine (ACC) affect TRPC6 expression in human monocytes. We observed that patients with chronic renal failure had significantly elevated HC levels and TRPC6 mRNA expression levels in monocytes compared with control subjects. We further observed that administration of HC or ACC significantly increased TRPC6 channel protein expression compared with control conditions. We, therefore, hypothesize that cysteine residues increase TRPC6 channel protein expression in humans. Antioxid. Redox Signal. 16, 452-457.
引用
收藏
页码:452 / 457
页数:6
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