
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NR3A CRISPR Activation Plasmid (h) | sc-403378-ACT | 20 µg | $397.00 |
GRIN3A encodes the NR3A subunit of N-methyl-D-aspartate (NMDA) receptors, an ionotropic glutamate receptor family that regulates calcium-permeable excitatory neurotransmission and synaptic plasticity. Incorporation of NR3A into receptor assemblies modulates channel properties, influencing neuronal excitability, activity-dependent signaling, and circuit maturation. Through effects on glutamatergic transmission, NR3A contributes to pathways governing neurodevelopment, synapse refinement, and experience-dependent remodeling. Altered GRIN3A expression or NMDA receptor subunit balance has been associated with neuropsychiatric and neurodevelopmental phenotypes, making it relevant for mechanistic studies of excitatory signaling dysregulation.
NR3A CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous GRIN3A expression without altering the underlying DNA sequence.
NR3A CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the GRIN3A locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the GRIN3A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous NR3A expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native GRIN3A locus and enabling the study of NR3A-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of NR3A pathway restoration in tumor cells with silenced or reduced GRIN3A expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.