ArticleThe Journal of biological chemistry2007
Common structural requirements for heptahelical domain function in class A and class C G protein-coupled receptors.
Article in The Journal of biological chemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 67 citations in OpenAlex.
- Functional Assessment of Calcium-Sensing Receptor Variants Confirms Familial Hypocalciuric Hypercalcemia.Journal of the Endocrine Society · 2022Article
- Review
- Class A and C GPCR Dimers in Neurodegenerative Diseases.Current neuropharmacology · 2022Review
- Structural Basis of GABACurrent topics in behavioral neurosciences · 2022Review
- Structural basis of GABANature · 2021Article
- Molecular mechanisms of metabotropic GABAScience advances · 2021Review
- Structural Characterization of Receptor-Receptor Interactions in the Allosteric Modulation of G Protein-Coupled Receptor (GPCR) Dimers.International journal of molecular sciences · 2021Review
- Calcium-sensing receptor signaling - How human disease informs biology.Current opinion in endocrine and metabolic research · 2021Article
- Calcium-sensing receptor residues with loss- and gain-of-function mutations are located in regions of conformational change and cause signalling bias.Human molecular genetics · 2018Article
- Helix α-3 inter-molecular salt bridges and conformational changes are essential for toxicity of Bacillus thuringiensis 3D-Cry toxin family.Scientific reports · 2018Article
- GPCRs and Signal Transducers: Interaction Stoichiometry.Trends in pharmacological sciences · 2018Review
- Structural biology of GABANeuropharmacology · 2018Review
- Metabotropic Glutamate Receptor 7: A New Therapeutic Target in Neurodevelopmental Disorders.Frontiers in molecular neuroscience · 2018Review
- An Intramolecular Salt Bridge in Bacillus thuringiensis Cry4Ba Toxin Is Involved in the Stability of Helix α-3, Which Is Needed for Oligomerization and Insecticidal Activity.Applied and environmental microbiology · 2017Article
- Analysis of positive and negative allosteric modulation in metabotropic glutamate receptors 4 and 5 with a dual ligand.Scientific reports · 2017Article
- Article
- Organization and functions of mGlu and GABANature · 2016Review
- Major ligand-induced rearrangement of the heptahelical domain interface in a GPCR dimer.Nature chemical biology · 2015Article
- GABAB receptor phosphorylation regulates KCTD12-induced K⁺ current desensitization.Biochemical pharmacology · 2014Article
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
G protein-coupled receptors (GPCRs) are key players in cell communication. Several classes of such receptors have been identified. Although all GPCRs possess a heptahelical domain directly activating G proteins, important structural and sequence differences within receptors from different classes suggested distinct activation mechanisms. Here we show that highly conserved charged residues likely involved in an interaction network between transmembrane domains (TM) 3 and 6 at the cytoplasmic side of class C GPCRs are critical for activation of the gamma-aminobutyric acid type B receptor. Indeed, the loss of function resulting from the mutation of the conserved lysine residue into aspartate or glutamate in the TM3 of gamma-aminobutyric acid type B(2) can be partly rescued by mutating the conserved acidic residue of TM6 into either lysine or arginine. In addition, mutation of the conserved lysine into an acidic residue leads to a nonfunctional receptor that displays a high agonist affinity. This is reminiscent of a similar ionic network that constitutes a lock stabilizing the inactive state of many class A rhodopsin-like GPCRs. These data reveal that despite their original structure, class C GPCRs share with class A receptors at least some common structural feature controlling G protein activation.
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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.