Conchon S, Monnot C, Teutsch B, Corvol P, Clauser E
Institut National de la Santé et de la Recherche Médicale Unité 36 Collège de France, Paris.
FEBS Lett. 1994 Aug 8;349(3):365-70. doi: 10.1016/0014-5793(94)00703-9.
The capacity of the angiotensin II (AngII) agonist [Sar1]AngII, the antagonist [Sar1-Ile8]AngII and the non-peptidic antagonist DuP753 to undergo receptor internalization were studied in Chinese hamster ovary cells expressing rat AngII type 1a or 1b receptors (AT1a or AT1b) or a mutant of AT1a (Asn74) unable to couple G-protein. In this expression system, the ligand-induced internalization of rat AT1a and AT1b are similar. Moreover, peptidic ligands, either the agonist or antagonist, induce a significant internalization of AT1 receptors, but the non-peptidic antagonist DuP753 is far less potent. Finally, the normal internalization of the mutant Asn74 demonstrates that receptor activation and G-protein coupling are not required for AT1a internalization.
在表达大鼠血管紧张素II 1a型或1b型受体（AT1a或AT1b）或无法偶联G蛋白的AT1a突变体（Asn74）的中国仓鼠卵巢细胞中，研究了血管紧张素II（AngII）激动剂[Sar1]AngII、拮抗剂[Sar1-Ile8]AngII和非肽类拮抗剂DuP753发生受体内化的能力。在该表达系统中，配体诱导的大鼠AT1a和AT1b内化相似。此外，肽类配体，无论是激动剂还是拮抗剂，均可诱导AT1受体发生显著内化，但非肽类拮抗剂DuP753的效力要低得多。最后，突变体Asn74的正常内化表明，AT1a内化不需要受体激活和G蛋白偶联。
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