|Application ||WB, IHC|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||105821 Da|
|Other Names||Gamma-aminobutyric acid type B receptor subunit 2, GABA-B receptor 2, GABA-B-R2, GABA-BR2, GABABR2, Gb2, G-protein coupled receptor 51, HG20, GABBR2, GPR51, GPRC3B|
|Target/Specificity||A synthetic peptide corresponding to residues near the C-terminus of human GABA(B) R2 was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||GABA(B) R2 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||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. 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.|
|Cellular Location||Cell membrane; Multi-pass membrane protein. Cell junction, synapse, postsynaptic cell membrane; Multi-pass membrane protein. Note=Coexpression of GABBR1 and GABBR2 is required for GABBR1 maturation and transport to the plasma membrane. In contrast, GABBR2 does not depend on GABBR1 for transport to the cell membrane|
|Tissue Location||Highly expressed in brain, especially in cerebral cortex, thalamus, hippocampus, frontal, occipital and temporal lobe, occipital pole and cerebellum, followed by corpus callosum, caudate nucleus, spinal cord, amygdala and medulla Weakly expressed in heart, testis and skeletal muscle|
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Provided below are standard protocols that you may find useful for product applications.
GABA (gamma-aminobutyric acid) is the main inhibitory neurotransmitter in the mammalian central nervous system, where it 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. Results indicate that, in vivo, functional brain GABA(B) receptors may be heterodimers composed of GABA(B)R1 and GABA(B)R2 (1). Identification of a functional homomeric GABABR2 coupled to adenylyl cyclase suggests that the complexity of GABAB pharmacological data is at least in part due to the presence of more than one receptor and opens avenues for future research leading to an understanding of metabotropic GABA receptor signal transduction mechanisms (2). The activity of GABA(B) R2 is mediated by G-proteins that inhibit adenylyl cyclase activity, stimulates phospholipase A2, activates potassium channels, inactivates voltage-dependent calcium-channels and modulates inositol phospholipids hydrolysis (3).
1. White JH, et al. Nature 396(6712): 679-82, 1998
2. Martin SC et al. Mol Cell Neurosci 13(3):180-91, 1999
3. Ng GY, et al. J Biol Chem 274(12):7607-10, 1999
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