ArticleHypertension (Dallas, Tex. : 1979)2005
Unconventional homologous internalization of the angiotensin II type-1 receptor induced by G-protein-independent signals.
Article in Hypertension (Dallas, Tex. : 1979), 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 40 citations in OpenAlex.
- Fast relaxation and desensitization of angiotensin II contraction in the pulmonary artery via AT1R and Akt-mediated phosphorylation of muscular eNOS.Pflugers Archiv : European journal of physiology · 2019Article
- G-Protein Coupled Receptor Targeting on Myeloid Cells in Atherosclerosis.Frontiers in pharmacology · 2019Review
- Klotho Ameliorates Medullary Fibrosis and Pressure Natriuresis in Hypertensive Rat Kidneys.Hypertension (Dallas, Tex. : 1979) · 2018Article
- Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology.Physiological reviews · 2018Review
- AT1 receptor signaling pathways in the cardiovascular system.Pharmacological research · 2017Review
- Angiotensin II increases glomerular permeability by β-arrestin mediated nephrin endocytosis.Scientific reports · 2016Article
- Targeting G protein coupled receptor-related pathways as emerging molecular therapies.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2015Review
- Angiotensin II Type 1 Receptor-Mediated Electrical Remodeling in Mouse Cardiac Myocytes.PloS one · 2015Article
- Biological and Pharmacological Aspects of the NK1-Receptor.BioMed research international · 2015Review
- Article
- G protein-coupled receptors in the hypothalamic paraventricular and supraoptic nuclei--serpentine gateways to neuroendocrine homeostasis.Frontiers in neuroendocrinology · 2012Review
- Biased signaling of the angiotensin II type 1 receptor can be mediated through distinct mechanisms.PloS one · 2010Article
- Site-specific cleavage of G protein-coupled receptor-engaged beta-arrestin. Influence of the AT1 receptor conformation on scissile site selection.The Journal of biological chemistry · 2008Article
- Beta-arrestins and heterotrimeric G-proteins: collaborators and competitors in signal transduction.British journal of pharmacology · 2008Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Internalization of a G-protein-coupled receptor (GPCR) is essential to the desensitization, endocytosis, and signal transduction of the receptor. It has been the general view that conventional homologous internalization of a GPCR requires activation of the G-protein(s) coupled to the receptor. However, whether and how GPCR-mediated G-protein-independent signals trigger receptor internalization remains unknown, although G-protein-independent internalization has been reported. Here we show that an angiotensin II (Ang II) type-1 (AT1) receptor mutant incapable of activating any G-protein still undergoes normal internalization. Substitution of Asp125 with Ala and Arg126 with Leu at the highly conserved DRY motif of the AT1 receptor disabled the ability of the receptor to activate G-proteins, as shown by various Ang II binding studies, GDP-GTP exchange, and inositol phosphate production assays. Surprisingly, the mutant internalized normally in the presence of Ang II and transactivated the epidermal growth factor receptor (EGFR). Similar to the wild-type receptor, overexpression of a dominant-negative K220R mutant GRK2 diminished the internalization of D125A-R126L but not the transactivation of EGFR. These data indicate that G-protein-independent specific signals may also trigger homologous internalizations of the AT1 receptor through beta-arrestin-dependent and -independent pathways, suggesting a possible mechanism for G-protein-independent activation of G-protein-coupled receptor kinases (GRKs). This may represent a general mechanism for triggering GPCR internalization.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.