ReviewMolecular pharmacology2008
Rich tapestry of G protein-coupled receptor signaling and regulatory mechanisms.
Review in Molecular pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Article
- Introduction: A Short History of Adrenoceptor Research.Handbook of experimental pharmacology · 2024Article
- Arrestin-mediated signaling: Is there a controversy?World journal of biological chemistry · 2018Review
- Permanent Photodynamic Cholecystokinin 1 Receptor Activation: Dimer-to-Monomer Conversion.Cellular and molecular neurobiology · 2018Article
- Drosophila Rhodopsin 7 can partially replace the structural role of Rhodopsin 1, but not its physiological function.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2017Article
- Rhodopsin 7-The unusual Rhodopsin in Drosophila.PeerJ · 2016Article
- Arrestins: Critical Players in Trafficking of Many GPCRs.Progress in molecular biology and translational science · 2015Review
- Rhodopsin TM6 can interact with two separate and distinct sites on arrestin: evidence for structural plasticity and multiple docking modes in arrestin-rhodopsin binding.Biochemistry · 2014Article
- Engineering visual arrestin-1 with special functional characteristics.The Journal of biological chemistry · 2013Article
- Regulation of the subcellular localization of the G-protein subunit regulator GPSM3 through direct association with 14-3-3 protein.The Journal of biological chemistry · 2012Article
- G-protein signaling modulator-3 regulates heterotrimeric G-protein dynamics through dual association with Gβ and Gαi protein subunits.The Journal of biological chemistry · 2012Article
- LGR6 is a high affinity receptor of R-spondins and potentially functions as a tumor suppressor.PloS one · 2012Article
- Reduced expression of G protein-coupled receptor kinases in schizophrenia but not in schizoaffective disorder.Neurobiology of disease · 2011Article
- Altered expression and function of regulator of G-protein signaling-17 (RGS17) in hepatocellular carcinoma.Cellular signalling · 2011Article
- A single mutation in arrestin-2 prevents ERK1/2 activation by reducing c-Raf1 binding.Biochemistry · 2011Article
- Autocrine signaling via A(1) adenosine receptors causes downregulation of M(2) receptors in adult rat atrial myocytes in vitro.Pflugers Archiv : European journal of physiology · 2011Article
- Custom-designed proteins as novel therapeutic tools? The case of arrestins.Expert reviews in molecular medicine · 2010Review
- Down-regulation of c-Cbl by morphine accounts for persistent ERK1/2 signaling in delta-opioid receptor-expressing HEK293 cells.The Journal of biological chemistry · 2009Article
- AT1 receptor-mediated uptake of angiotensin II and NHE-3 expression in proximal tubule cells through a microtubule-dependent endocytic pathway.American journal of physiology. Renal physiology · 2009Article
- Structural features of mammalian histidine decarboxylase reveal the basis for specific inhibition.British journal of pharmacology · 2009Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
G protein-coupled receptors (GPCRs) are the largest family of signaling proteins and the most common therapeutic targets. In the last 2 decades, impressive progress in the understanding of GPCR function has been achieved, driven largely by the idea of similarity of the molecular mechanisms underlying their signaling and regulation. However, recent comprehensive studies of signaling and trafficking of several GPCR subtypes, including endogenous M3 muscarinic and H1 histamine receptor and expressed cysteinyl leukotriene type 1 receptor in human embryonic kidney 293 cells, clearly demonstrate that each receptor is regulated by a unique set of molecular mechanisms involving different players. These data indicate that the "gold mine" of similarities is nearly exhausted and that extrapolation from one receptor to another is as likely to be misleading as illuminating. Further progress in the field requires careful analysis of the regulation of individual GPCR subtypes in defined cellular context. In this issue of Molecular Pharmacology, Luo et al. (p. 338) describe a complex pattern of the regulation of M3 muscarinic receptor signaling.
Indexed as
Identifiers
What OpenQuestion holds
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.