Aliases for GABBR1 Gene
External Ids for GABBR1 Gene
Gamma-aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the mammalian central nervous system. GABA exerts its effects through ionotropic [GABA(A/C)] receptors, to produce fast synaptic inhibition, and metabotropic [GABA(B)] receptors, to produce slow, prolonged inhibitory signals. The GABA(B) receptor consists of a heterodimer of two related 7-transmembrane receptors, GABA(B) receptor 1 and GABA(B) receptor 2. The GABA(B) receptor 1 gene is mapped to chromosome 6p21.3 within the HLA class I region close to the HLA-F gene. Susceptibility loci for multiple sclerosis, epilepsy, and schizophrenia have also been mapped in this region. Alternative splicing of this gene generates multiple transcript variants. [provided by RefSeq, Jun 2009]
GeneCards Summary for GABBR1 Gene
GABBR1 (Gamma-Aminobutyric Acid (GABA) B Receptor, 1) is a Protein Coding gene. Diseases associated with GABBR1 include persistent vegetative state and withdrawal disorder. Among its related pathways are Signaling by GPCR and Signaling by GPCR. GO annotations related to this gene include G-protein coupled GABA receptor activity. An important paralog of this gene is GPR156.
UniProtKB/Swiss-Prot for GABBR1 Gene
Component of a heterodimeric G-protein coupled receptor for GABA, formed by GABBR1 and GABBR2. Within the heterodimeric GABA receptor, only GABBR1 seems to bind agonists, while GABBR2 mediates coupling to G proteins. Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of down-stream effectors, such as adenylate cyclase. Signaling inhibits adenylate cyclase, stimulates phospholipase A2, activates potassium channels, inactivates voltage-dependent calcium-channels and modulates inositol phospholipid hydrolysis. Calcium is required for high affinity binding to GABA. Plays a critical role in the fine-tuning of inhibitory synaptic transmission. Pre-synaptic GABA receptor inhibits neurotransmitter release by down-regulating high-voltage activated calcium channels, whereas postsynaptic GABA receptor decreases neuronal excitability by activating a prominent inwardly rectifying potassium (Kir) conductance that underlies the late inhibitory postsynaptic potentials. Not only implicated in synaptic inhibition but also in hippocampal long-term potentiation, slow wave sleep, muscle relaxation and antinociception. Activated by (-)-baclofen, cgp27492 and blocked by phaclofen
Isoform 1E may regulate the formation of functional GABBR1/GABBR2 heterodimers by competing for GABBR2 binding. This could explain the observation that certain small molecule ligands exhibit differential affinity for central versus peripheral sites
GABAB receptors are metabotropic G-protein-coupled receptors responsible for mediating the inhibitory effects of GABA alongside ionotropic GABAA and GABAC receptors. They exist as heterodimers of GABAB1 and GABAB2 subunits and the presence of both subunits is required for receptor function. When GABAB1 is expressed alone it is non-functional and is not transported to the cell membrane. The GABAB1 subunit is responsible for binding GABA while the GABAB2 subunit interacts with the G protein. The two subunits interact allosterically, GABA increases coupling of GABAB2 to G proteins and GABAB2 increases agonist binding to GABAB1. GABAB receptors are coupled to Ca2+ and K+ channels.