血管紧张素II AT1受体在进化过程中的结构和功能。

Journal de la Societe de biologie Pub Date : 2009-01-01 Epub Date: 2010-02-01 DOI:10.1051/jbio/2009033
Colette Auzan, Eric Clauser
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引用次数: 0

摘要

血管紧张素II AT1受体是一种G蛋白偶联受体,它能传导这种血管活性肽的生理效应(血管收缩、醛固酮分泌)。从进化的角度来看,这种受体在脊椎动物发育的早期就出现了,因为它存在于软骨鱼中。它已经在啮齿类动物身上复制,但对其功能没有任何影响。血管紧张素AT2受体(其功能仍有争议)不太可能与AT1受体的共同祖先血管紧张素受体分离。通过AT1受体序列的定点诱变,已经发现了许多激活或失活的点突变。然而,这种自然突变在人类疾病的发生或表型特征的多样性中似乎并不常见。
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[Structure and functions of the angiotensin II AT1 receptors during evolution].

Angiotensin II AT1 receptor is a G protein coupled receptor, which transduces the physiological effects (vasoconstriction, aldosterone secretion) f this vasoactive peptide. On an evolutionary point of view, this receptor has appeared early in the development of vertebrates, since it is present in cartilagenous fish. It has been duplicated in rodents without any consequence on its functions. It is unlikely that the angiotensin AT2 receptor, whose functions are still debated, has diverged from a common ancestral angiotensin receptor with the AT1 receptor. Numerous activating or inactivating point mutations have been identified by site-directed mutagenesis of the AT1 receptor sequence. However, such natural mutations do not appear to be frequent in the genesis of human diseases or in the diversity of phenotypic traits.

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