ArticleProceedings of the National Academy of Sciences of the United States of America2016
Mapping physiological G protein-coupled receptor signaling pathways reveals a role for receptor phosphorylation in airway contraction.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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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Who cites it
26 citing papers in PubMed, 50 citations in OpenAlex.
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- A golden age of muscarinic acetylcholine receptor modulation in neurological diseases.Nature reviews. Drug discovery · 2024Review
- GRespiratory research · 2024Review
- Interleukin 31 receptor α promotes smooth muscle cell contraction and airway hyperresponsiveness in asthma.Nature communications · 2023Article
- Middle-Down Mass Spectrometry Reveals Activity-Modifying Phosphorylation Barcode in a Class C G Protein-Coupled Receptor.Journal of the American Chemical Society · 2022Article
- New Tricks for an Old Dog: Biased GPCR Agonism of an M4 Muscarinic Acetylcholine Receptor Antagonist in Airway Smooth Muscle Cells.American journal of respiratory cell and molecular biology · 2022Article
- PD 102807 Induces M3 mAChR-Dependent GRK-/Arrestin-Biased Signaling in Airway Smooth Muscle Cells.American journal of respiratory cell and molecular biology · 2022Article
- G protein-biased GPR3 signaling ameliorates amyloid pathology in a preclinical Alzheimer's disease mouse model.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Biased M1 muscarinic receptor mutant mice show accelerated progression of prion neurodegenerative disease.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Diacylglycerol Kinase Inhibition Reduces Airway Contraction by Negative Feedback Regulation of Gq-Signaling.American journal of respiratory cell and molecular biology · 2021Article
- RGS12 is a novel tumor suppressor in osteosarcoma that inhibits YAP-TEAD1-Ezrin signaling.Oncogene · 2021Article
- Targeting G protein-coupled receptor kinases (GRKs) to G protein-coupled receptors.Current opinion in endocrine and metabolic research · 2021Article
- Biased M1-muscarinic-receptor-mutant mice inform the design of next-generation drugs.Nature chemical biology · 2020Article
- G Protein-Coupled Receptors in Asthma Therapy: Pharmacology and Drug Action.Pharmacological reviews · 2020Review
- Cholinergic synapse pathway gene polymorphisms associated with allergen-induced late asthmatic responses.ERJ open research · 2019Article
- Updates in the function and regulation of αBritish journal of pharmacology · 2019Review
- Identification and pharmacological profile of SPP1, a potent, functionally selective and brain penetrant agonist at muscarinic MBritish journal of pharmacology · 2019Article
- Neuropeptides in asthma, chronic obstructive pulmonary disease and cystic fibrosis.Respiratory research · 2018Review
- Selective inhibition of histamine-evoked CaCell calcium · 2018Article
- GαBritish journal of pharmacology · 2017Article
Corrections and comments
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Authors and funding
18 authors at 6 institutions in 3 countries.
Funding
Abstract
G protein-coupled receptors (GPCRs) are known to initiate a plethora of signaling pathways in vitro. However, it is unclear which of these pathways are engaged to mediate physiological responses. Here, we examine the distinct roles of Gq/11-dependent signaling and receptor phosphorylation-dependent signaling in bronchial airway contraction and lung function regulated through the M3-muscarinic acetylcholine receptor (M3-mAChR). By using a genetically engineered mouse expressing a G protein-biased M3-mAChR mutant, we reveal the first evidence, to our knowledge, of a role for M3-mAChR phosphorylation in bronchial smooth muscle contraction in health and in a disease state with relevance to human asthma. Furthermore, this mouse model can be used to distinguish the physiological responses that are regulated by M3-mAChR phosphorylation (which include control of lung function) from those responses that are downstream of G protein signaling. In this way, we present an approach by which to predict the physiological/therapeutic outcome of M3-mAChR-biased ligands with important implications for drug discovery.
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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.