Molecular mechanisms of angiotensin II receptor internalization

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43 Citations (Scopus)

Abstract

Angiotensin II (AngII) initiates cellular responses by activation of type 1 (AT1) and type 2 (AT2) angiotensin receptors. Both AT1 and AT2 receptors have seven transmembrane structures characteristic of G protein- coupled receptors, but only the AT1 receptor undergoes rapid internalization upon agonist binding. In addition to the agonist hormone, the peptide antagonist [Sar1,Ile8]AngII can also induce internalization of the AT(1a) receptor expressed in mammalian cell lines, but the nonpeptide AT1 receptor blocker losartan does not internalize. AT1 receptor internalization occurs via clathrin-coated pits, but there is evidence that, in contrast to the internalization of other G protein-coupled receptors, the internalization of the AT1 receptor is independent of dynamin and β-arrestin. Mutagenesis studies demonstrated that AT1 receptor internalization requires two regions in the cytoplasmic tail of the receptor, but it is independent of G protein activation. The dependence of AT1 receptor internalization on the presence of a serine-threonine-rich region suggests that phosphorylation of the receptor tail may regulate the internalization process. The possible role of AT1 receptor internalization in sustained signal generation has been suggested, but its relationship to nuclear AngII receptors is not completely understood.

Original languageEnglish
JournalJournal of the American Society of Nephrology
Volume10
Issue number1 SUPPL. 11
Publication statusPublished - Jan 1999

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Angiotensin Receptors
G-Protein-Coupled Receptors
Angiotensin II
Angiotensin Type 2 Receptor
Dynamins
Arrestin
Hormone Antagonists
Clathrin
Angiotensin Type 1 Receptor
Losartan
Threonine
Cytoplasmic and Nuclear Receptors
GTP-Binding Proteins
Mutagenesis
Serine
Phosphorylation
Cell Line

ASJC Scopus subject areas

  • Nephrology

Cite this

Molecular mechanisms of angiotensin II receptor internalization. / Hunyady, L.

In: Journal of the American Society of Nephrology, Vol. 10, No. 1 SUPPL. 11, 01.1999.

Research output: Contribution to journalArticle

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