HEK293 TREX Human GluN1a/GluN2D Stable Cell
Item | Cat# | Price |
Stable Cell Line | SNB-I-0041A | $19,800 |
Compound Test Services | CT-001 | $1,850 per 384w plate (Up To 16 cpds Dose) |
Product Description
The N-methyl-D-aspartate receptor (NMDA receptor or NMDAR) is a subtype of ionotropic glutamate receptor that plays a critical role in synaptic transmission, plasticity, and excitatory signaling in the central nervous system. It functions as a ligand-gated and voltage-dependent cation channel permeable to calcium, sodium, and potassium ions. Activation of NMDARs requires both glutamate binding and co-agonist glycine (or D-serine), as well as relief from magnesium ion block through membrane depolarization. Structurally, NMDA receptors are heterotetramers typically composed of GluN1 and GluN2 (A–D) subunits, which determine their functional and pharmacological properties. NMDAR-mediated calcium influx is essential for learning, memory, and long-term potentiation (LTP), but excessive activation can lead to excitotoxicity and neuronal injury, contributing to neurological disorders such as stroke, Alzheimer’s disease, and epilepsy.
Screeningbio’s GluN1a/GluN2D cell line express non-tag full length human NMDA receptor GluN1a and GluN2D subunit in HEK293 cell. When induced and activated, cell line response to extracellular stimuli (e.g. Glutamate) and result in channel opening and calcium influx. Increase of intercellular calcium was detected by calcium sensitive dye.
Product Specifications
Target Type | Ion Channel |
Species | Human |
HGNC Symbol | NMDA |
Accession Number | NM_007327 (GluN1a), NM_000827 (GluN2D) |
Parental Line | HEK293 |
Lot# | See Vial |
Storage | Liquid Nitrogen |
Data
![Human GluN1a/GluN2D Blocker Assay. HEK293 TREX Human GluN1a/GluN2D cells were seeded in 384-well plate and incubated at 30oC in 5% CO2 incubator for 24 hours before running the assay. The cells were treated with the reference blockers and stimulated by activator Capsaicin. The assay was run based on FLIPR Calcium 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/cbf7de_96ddf2ba68284827b51ce026398460ec~mv2.png/v1/fill/w_76,h_75,al_c,q_85,usm_0.66_1.00_0.01,blur_2,enc_auto/cbf7de_96ddf2ba68284827b51ce026398460ec~mv2.png)
Target Background
The N-methyl-D-aspartate receptor (NMDAR) subunit GluN2D, encoded by the GRIN2D gene, is one of the four GluN2 subunits (A–D) that combine with GluN1 to form functional heterotetrameric NMDARs. GluN2D-containing receptors exhibit distinct kinetic and pharmacological features that set them apart from other NMDAR subtypes, contributing to their specialized roles in neuronal signaling and development.
GluN2D subunits are characterized by exceptionally high affinity for glutamate and glycine, very slow deactivation kinetics, and minimal voltage-dependent Mg²⁺ blockade. These properties allow GluN2D-containing receptors to sustain prolonged excitatory currents even after transient glutamate exposure, facilitating extended calcium signaling at low synaptic activity levels. Such slow kinetics make GluN2D particularly important for shaping excitatory postsynaptic potentials and maintaining synaptic plasticity in specific neuronal populations.
During early brain development, GluN2D is widely expressed throughout the central nervous system, but in the mature brain, its expression becomes restricted to regions such as the midbrain, diencephalon, and brainstem, including dopaminergic neurons in the substantia nigra and GABAergic interneurons. This distribution suggests that GluN2D plays a critical role in modulating inhibitory–excitatory balance, motor control, and neuromodulatory pathways.
Altered GluN2D function has been associated with neurological disorders including epilepsy, Parkinson’s disease, and schizophrenia. From a pharmacological standpoint, GluN2D-selective antagonists or positive allosteric modulators are being explored as potential therapeutic agents for treating neurodegenerative and psychiatric diseases, as they allow selective modulation of NMDAR signaling while minimizing excitotoxic side effects seen with non-selective NMDA blockers.