ArticleThe Journal of biological chemistry2002
A single subunit (GB2) is required for G-protein activation by the heterodimeric GABA(B) receptor.
Article in The Journal of biological chemistry, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 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
74 citing papers in PubMed, 196 citations in OpenAlex.
- GABA-independent activation of GABANature communications · 2025Article
- Both calcium-sensing receptor intracellular C-terminal domains support homodimer signaling.Molecular pharmacology · 2025Article
- Structural Basis of GABAAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Smooth operator(s): dialing up and down neurotransmitter responses by G-protein regulators.Trends in cell biology · 2025Review
- Article
- The olfactory Olfr-78/51E2 receptor interacts with the adenosine AFrontiers in pharmacology · 2023Article
- Structural Basis of GABACurrent topics in behavioral neurosciences · 2022Review
- Class A and C GPCR Dimers in Neurodegenerative Diseases.Current neuropharmacology · 2022Review
- GABACurrent topics in behavioral neurosciences · 2022Review
- Mechanisms and Regulation of Neuronal GABACurrent topics in behavioral neurosciences · 2022Review
- Structural basis of GABANature · 2021Article
- Structure and function of adenosine receptor heteromers.Cellular and molecular life sciences : CMLS · 2021Review
- 5-Hydroxytryptamine, Glutamate, and ATP: Much More Than Neurotransmitters.Frontiers in cell and developmental biology · 2021Article
- Structure of human GABANature · 2020Article
- Article
- The GABAMolecules (Basel, Switzerland) · 2020Review
- Cryo-EM structures of inactive and active GABACell research · 2020Article
- Cross-modal reaction of auditory and visual cortices after long-term bilateral hearing deprivation in the rat.Brain structure & function · 2020Article
- Structural basis for auxiliary subunit KCTD16 regulation of the GABAProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Bioluminescence Resonance Energy Transfer as a Method to Study Protein-Protein Interactions: Application to G Protein Coupled Receptor Biology.Molecules (Basel, Switzerland) · 2019Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although G-protein-coupled receptors (GPCRs) have been shown to assemble into functional homo or heteromers, the role of each protomer in G-protein activation is not known. Among the GPCRs, the gamma-aminobutyric acid (GABA) type B receptor (GABA(B)R) is the only one known so far that needs two subunits, GB1 and GB2, to function. The GB1 subunit contains the GABA binding site but is unable to activate G-proteins alone. In contrast the GB2 subunit, which does not bind GABA, has an heptahelical domain able to activate G-proteins when assembled into homodimers (Galvez, T., Duthey, B., Kniazeff, J., Blahos, J., Rovelli, G., Bettler, B., Prézeau, L., and Pin, J.-P. (2001) EMBO J. 20, 2152-2159). In the present study, we have examined the role of each subunit within the GB1-GB2 heteromer, in G-protein coupling. To that end, point mutations in the highly conserved third intracellular loop known to prevent G-protein activation of the related Ca-sensing or metabotropic glutamate receptors were introduced into GB1 and GB2. One mutation, L686P introduced in GB2 prevents the formation of a functional receptor, even though the heteromer reaches the cell surface, and even though the mutated subunit still associates with GB1 and increases GABA affinity on GB1. This was observed either in HEK293 cells where the activation of the G-protein was assessed by measurement of inositol phosphate accumulation, or in cultured neurons where the inhibition of the Ca(2+) channel current was measured. In contrast, the same mutation when introduced into GB1 does not modify the G-protein coupling properties of the heteromeric GABA(B) receptor either in HEK293 cells or in neurons. Accordingly, whereas in all GPCRs the same protein is responsible for both agonist binding and G-protein activation, these two functions are assumed by two distinct subunits in the GABA(B) heteromer: one subunit, GB1, binds the agonists whereas the other, GB2, activates the G-protein. This illustrates the importance of a single subunit for G-protein activation within a dimeric receptor.
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.