ArticlePloS one2012
GABAB receptor subunit GB1 at the cell surface independently activates ERK1/2 through IGF-1R transactivation.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Activation of GABBR1 by New Ligand Valerate Transcriptionally Regulates ATF4-NRF2-CXCL13 Axis Mediating CD8International journal of biological sciences · 2026Article
- The GABA and GABA-Receptor System in Inflammation, Anti-Tumor Immune Responses, and COVID-19.Biomedicines · 2023Review
- Gamma-Aminobutyric Acid (GABA) Promotes Growth in Zebrafish Larvae by Inducing IGF-1 Expression via GABAInternational journal of molecular sciences · 2021Article
- GABABiomedicines · 2021Article
- Unique and independent role of the GABAGenes & diseases · 2021Article
- Impaired Expression of GABA Signaling Components in the Alzheimer's Disease Middle Temporal Gyrus.International journal of molecular sciences · 2020Article
- Cryo-EM structures of inactive and active GABACell research · 2020Article
- A Review of the Potential Mechanisms of Action of Baclofen in Alcohol Use Disorder.Frontiers in psychiatry · 2018Review
- Towards a Better Understanding of GABAergic Remodeling in Alzheimer's Disease.International journal of molecular sciences · 2017Review
- Allosteric control of an asymmetric transduction in a G protein-coupled receptor heterodimer.eLife · 2017Article
- Effect ofExperimental and therapeutic medicine · 2016Article
- Chronic baclofen desensitizes GABA(B)-mediated G-protein activation and stimulates phosphorylation of kinases in mesocorticolimbic rat brain.Neuropharmacology · 2015Article
- Complex GABAB receptor complexes: how to generate multiple functionally distinct units from a single receptor.Frontiers in pharmacology · 2014Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFunctional GABA(B) receptor is believed to require hetero-dimerization between GABA(B1) (GB1) and GABA(B2) (GB2) subunits. The GB1 extracellular domain is required for ligand binding, and the GB2 trans-membrane domain is responsible for coupling to G proteins. Atypical GABA(B) receptor responses observed in GB2-deficient mice suggested that GB1 may have activity in the absence of GB2. However the underlying mechanisms remain poorly characterized. METHODOLOGY/PRINCIPAL
findingsHere, by using cells overexpressing a GB1 mutant (GB1asa) with the ability to translocate to the cell surface in the absence of GB2, we show that GABA(B) receptor agonists, such as GABA and Baclofen, can induce ERK1/2 phosphorylation in the absence of GB2. Furthermore, we demonstrate that GB1asa induces ERK1/2 phosphorylation through Gi/o proteins and PLC dependent IGF-1R transactivation. CONCLUSIONS/SIGNIFICANCE: Our data suggest that GB1 may form a functional receptor at the cell surface in the absence of GB2.
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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.