ArticleThe Journal of biological chemistry2014
Proteasomal degradation of γ-aminobutyric acidB receptors is mediated by the interaction of the GABAB2 C terminus with the proteasomal ATPase Rtp6 and regulated by neuronal activity.
Article in The Journal of biological chemistry, 2014. 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.
- Investigating the neuronal role of the proteasomal ATPase subunit gene PSMC5 in neurodevelopmental proteasomopathies.Nature communications · 2025Article
- Restoring Homeostasis: Treating Amyotrophic Lateral Sclerosis by Resolving Dynamic Regulatory Instability.International journal of molecular sciences · 2025Article
- The E3 ubiquitin ligase MARCH1 mediates downregulation of plasma membrane GABAScientific reports · 2025Article
- Substrate-specific effects of natural genetic variation on proteasome activity.PLoS genetics · 2023Article
- Genome-wide effects of social status on DNA methylation in the brain of a cichlid fish, Astatotilapia burtoni.BMC genomics · 2019Article
- CaMolecular neurobiology · 2019Article
- Membrane Protein Quantity Control at the Endoplasmic Reticulum.The Journal of membrane biology · 2017Review
- Lys-63-linked Ubiquitination of γ-Aminobutyric Acid (GABA), Type B1, at Multiple Sites by the E3 Ligase Mind Bomb-2 Targets GABAB Receptors to Lysosomal Degradation.The Journal of biological chemistry · 2016Article
- Phosphorylation state-dependent modulation of spinal glycine receptors alleviates inflammatory pain.The Journal of clinical investigation · 2016Article
- Post-endocytotic Deubiquitination and Degradation of the Metabotropic γ-Aminobutyric Acid Receptor by the Ubiquitin-specific Protease 14.The Journal of biological chemistry · 2016Article
- Protein Expression of Proteasome Subunits in Elderly Patients with Schizophrenia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
- Ischemia-like oxygen and glucose deprivation mediates down-regulation of cell surface γ-aminobutyric acidB receptors via the endoplasmic reticulum (ER) stress-induced transcription factor CCAAT/enhancer-binding protein (C/EBP)-homologous protein (CHOP).The Journal of biological chemistry · 2014Article
- Ubiquitin-proteasome dependent degradation of GABAAα1 in autism spectrum disorder.Molecular autism · 2014Article
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Authors and funding
2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Regulation of cell surface expression of neurotransmitter receptors is crucial for determining synaptic strength and plasticity, but the underlying mechanisms are not well understood. We previously showed that proteasomal degradation of GABAB receptors via the endoplasmic reticulum (ER)-associated protein degradation (ERAD) machinery determines the number of cell surface GABAB receptors and thereby GABAB receptor-mediated neuronal inhibition. Here, we show that proteasomal degradation of GABAB receptors requires the interaction of the GABAB2 C terminus with the proteasomal AAA-ATPase Rpt6. A mutant of Rpt6 lacking ATPase activity prevented degradation of GABAB receptors but not the removal of Lys(48)-linked ubiquitin from GABAB2. Blocking ERAD activity diminished the interaction of Rtp6 with GABAB receptors resulting in increased total as well as cell surface expression of GABAB receptors. Modulating neuronal activity affected proteasomal activity and correspondingly the interaction level of Rpt6 with GABAB2. This resulted in altered cell surface expression of the receptors. Thus, neuronal activity-dependent proteasomal degradation of GABAB receptors by the ERAD machinery is a potent mechanism regulating the number of GABAB receptors available for signaling and is expected to contribute to homeostatic neuronal plasticity.
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