CHO-K1 Human Glycine Receptor α3 Stable Cell
Item | Cat# | Price |
Stable Cell Line | SNB-I-0028A | $19,800 |
Compound Test Services | CT-001 | $1,850 per 384w plate (Up To 16 cpds Dose) |
Product Description
The Glycine Receptor (GlyR) is a ligand-gated chloride ion channel that plays a central role in inhibitory neurotransmission within the spinal cord, brainstem, and retina. Belonging to the Cys-loop receptor superfamily, which also includes GABAa, nicotinic acetylcholine, and serotonin 5-HT3 receptors, GlyR mediates rapid synaptic inhibition through the binding of its endogenous ligand glycine. Activation of GlyR triggers chloride ion influx, leading to membrane hyperpolarization and reduced neuronal excitability.
Structurally, GlyR is a pentameric complex typically composed of α (α1–α4) and β subunits, with the α subunits forming the ligand-binding sites. The β subunit is essential for anchoring the receptor to the postsynaptic scaffold via interaction with gephyrin, ensuring proper synaptic localization. Genetic mutations in GLRA1 or GLRB can disrupt receptor function and are associated with hyperekplexia (startle disease), a neurological disorder characterized by exaggerated motor responses to stimuli.
GlyR has become a valuable model for understanding ligand-gated ion channel mechanisms, synaptic inhibition, and allosteric modulation. Its pharmacological relevance extends to studies of anesthetic action, convulsant toxicity, and the development of therapeutic modulators targeting inhibitory neurotransmission in neurological diseases.
Screeningbio’s Glycine α3 cell line stable express non-tag full length Glycine receptor α3 subunit in CHO-K1 cell. When activated, Glycine α3 cell line response to extracellular stimuli (e.g. glycine) and result in channel opening and change of membrane potential. The change of membrane potential will be detected by membrane potential kit.
Product Specifications
Target Type | Ion Channel |
Species | Human |
HGNC Symbol | GlyR |
Accession Number | NM_006529 (α3 subunit) |
Parental Line | CHO-K1 |
Lot# | See Vial |
Storage | Liquid Nitrogen |
Data
![Human Glycine Receptor Blocker Assay. CHO-K1 Human Glycine Receptor α3 cell were seeded in 384-well plate and incubated at 37oC in 5% CO2 incubator for 24 hours before running the assay. The cells were treated with the reference blockers and stimulated by EC80 concentration of activator. The assay was run based on FLIPR membrane potential assay protocol. Non-linear regression was used to plot activity changes vs. [Compound, M], and EC50 /IC50 values were determined, using GraphPad Prism software.](https://static.wixstatic.com/media/56275b_cb7158b40f754f138f827a0d2dabdab2~mv2.png/v1/fill/w_76,h_75,al_c,q_85,usm_0.66_1.00_0.01,blur_2,enc_auto/56275b_cb7158b40f754f138f827a0d2dabdab2~mv2.png)
Target Background
The glycine receptor (GlyR) is a ligand-gated chloride channel that belongs to the Cys-loop receptor superfamily, which also includes GABAA_AA, nicotinic acetylcholine, and serotonin type 3 receptors. Structurally, GlyR is a pentameric complex composed of α and β subunits that form a central pore selectively permeable to chloride ions. Binding of the inhibitory neurotransmitter glycine to the extracellular domain triggers conformational changes that open the channel, resulting in chloride influx and membrane hyperpolarization, thereby reducing neuronal excitability.
GlyR is predominantly expressed in the spinal cord, brainstem, and other regions of the central nervous system, where it mediates fast inhibitory neurotransmission. It plays a key role in motor control, sensory processing, and the modulation of pain and reflex pathways. In the developing nervous system, glycinergic signaling also contributes to synapse formation and neuronal differentiation.
Dysfunction or genetic mutations of GlyR subunits are implicated in neurological disorders such as hyperekplexia (startle disease), chronic pain, epilepsy, and certain motor disorders. Pharmacological agents that modulate GlyR activity have potential therapeutic applications in pain management, spasticity, and neurodegenerative diseases. Due to its well-defined structure, rapid inhibitory signaling, and critical role in spinal neurotransmission, GlyR serves as a fundamental model for understanding inhibitory synaptic mechanisms in the central nervous system.