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在血管紧张素II刺激的大鼠肾上腺球状带细胞中,I型血管紧张素II受体(AT1)的内化是蛋白激酶C激活所必需的,但对于肌醇三磷酸的释放并非必需。

Internalization of the type I angiotensin II receptor (AT1) is required for protein kinase C activation but not for inositol trisphosphate release in the angiotensin II stimulated rat adrenal zona glomerulosa cell.

作者信息

Kapas S, Hinson J P, Puddefoot J R, Ho M M, Vinson G P

机构信息

Department of Biochemistry, Queen Mary & Westfield College, London, United Kingdom.

出版信息

Biochem Biophys Res Commun. 1994 Nov 15;204(3):1292-8. doi: 10.1006/bbrc.1994.2603.

Abstract

A specific antibody, 6313/G2, to the N-terminus of the angiotensin II type I (AT1) receptor causes retention of the AT1 receptor in the plasma membrane of rat adrenal zona glomerulosa cells and stimulates steroidogenesis and inositol trisphosphate (IP3) release. Its effects are not significantly additive with those of angiotensin. In contrast, 6313/G2 completely inhibits angiotensin induced translocation of protein kinase C to the membrane fraction, although alone it has no effect. The data suggest that IP3 linked events, such as steroidogenesis, do not require receptor internalization, but protein kinase C activation does. They also confirm that protein kinase C activation is not required for stimulation of steroidogenesis in rat dispersed glomerulosa cells.

摘要

一种针对血管紧张素II 1型(AT1)受体N端的特异性抗体6313/G2,可使AT1受体滞留在大鼠肾上腺球状带细胞的质膜中,并刺激类固醇生成和肌醇三磷酸(IP3)释放。其作用与血管紧张素的作用无明显叠加。相反,6313/G2完全抑制血管紧张素诱导的蛋白激酶C向膜组分的转位,尽管其单独作用时无此效应。数据表明,与类固醇生成等IP3相关事件不需要受体内化,但蛋白激酶C激活需要。它们还证实,在大鼠分散的球状带细胞中,刺激类固醇生成不需要蛋白激酶C激活。

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