期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 391, 期 1, 页码 85-90出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2009.11.008
关键词
Angiotensin II receptors; Signal cross-talk; Dimerization; Inositol phosphate production; Phospholipase C
资金
- Ministry of Education, Culture, Sports, Science and Technology, Japan [18590916, 21591065]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL057470] Funding Source: NIH RePORTER
Although angiotensin II (Ang II) binds to Ang II type I (AT(1)) and type 2 (AT(2)) receptors. AT(1) and AT(2) receptors have antagonistic actions with regard to cell signaling. The molecular mechanisms that underlie this antagonism are not well understood. We examined AT(1) and AT(2) receptor-induced signal cross-talk in the cytoplasm and the importance of the hetero-dimerization of AT(1) receptor with AT(2) receptor on the cell surface. AT(1) and AT(2) receptors showed antagonistic effects toward inositol phosphate production AT(1) receptors mainly formed homo-dimers, rather than hetero-dimers with AT(2) receptor, on the cell surface as determined by immunoprecipitation, and subsequently induced cell signals AT(2) receptor mainly formed homo-dimers. rather than hetero-dimers with AT(1) receptor, on the cell surface. The expression levels of homo-dimerized AT(1) receptor or AT(2) receptor on the cell surface did not change after treatment with Ang II, the AT(1) receptor antagonist telmisartan or the AT(2) receptor antagonist PD123319 Finally, AT(1) and AT(2) receptor-induced signals antagonized phospholipase C-beta(3) phosphorylation in conclusion, Ang II-induced AT(1) receptor signals may be mainly blocked by AT(2) receptor signals through their negative cross-talk in the cytoplasm rather than by the hetero-dimerization of both receptors on the cell surface. The proper balance of the expression levels of AT(1) and AT(2) receptors might be critical for the antagonistic action between these receptors. (C) 2009 Elsevier Inc All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据