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蛋白激酶C能迅速上调培养的大鼠肠上皮(RIE-1)细胞上AT1血管紧张素受体的数量。

Protein kinase C rapidly up-regulates the number of AT1 angiotensin receptors on cultured rat intestinal epithelial (RIE-1) cells.

作者信息

Smith R D

机构信息

Department of Clinical Biochemistry, Addenbrooke's Hospital, Cambridge, UK.

出版信息

FEBS Lett. 1994 Jul 4;348(1):51-4. doi: 10.1016/0014-5793(94)00584-2.

Abstract

Addition of 12-O-tetradecanoylphorbol-13-acetate to RIE-1 rat intestinal epithelial cells stimulated a rapid (mean 3-fold) increase in the subsequent binding of 125I-labelled angiotensin II which was reversed or prevented when cellular protein kinase C was depleted. The increased binding was due, in part, to an up-regulation in the number of AT1 angiotensin receptors on RIE-1 cells, without any significant change in their binding affinity. Since this rapid up-regulation was independent of receptor synthesis, it may result from an increased availability (to extracellular ligand) of performed, but previously 'cryptic', AT1 angiotensin receptors.

摘要

向RIE-1大鼠肠上皮细胞中添加12-O-十四烷酰佛波醇-13-乙酸酯,可刺激随后125I标记的血管紧张素II的结合迅速增加(平均增加3倍),而当细胞蛋白激酶C被耗尽时,这种增加会被逆转或阻止。结合增加部分是由于RIE-1细胞上AT1血管紧张素受体数量的上调,而其结合亲和力没有任何显著变化。由于这种快速上调独立于受体合成,它可能是由于已形成但先前“隐蔽”的AT1血管紧张素受体对细胞外配体的可及性增加所致。

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