NR3A CRISPR/Cas9 KO Plasmid (h): sc-403378
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NR3A CRISPR/Cas9 Knockout (KO) Plasmid (h) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the NR3A genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NR3A CRISPR/Cas9 KO Plasmid (h) | sc-403378 | 20 µg | $397.00 |
Overview
GRIN3A encodes the human NR3A subunit of N-methyl-D-aspartate (NMDA) receptors, a glutamate-gated ion channel complex that shapes synaptic transmission and neuronal excitability. Incorporation of NR3A into NMDA receptors alters channel properties, including reduced Ca2+ permeability and modified Mg2+ block, thereby influencing activity-dependent synaptic remodeling and plasticity. GRIN3A expression is developmentally regulated and is implicated in processes such as excitatory/inhibitory balance, dendritic maturation, and circuit refinement. Dysregulated NMDA receptor subunit composition, including altered NR3A levels, has been associated with neurodevelopmental and neuropsychiatric phenotypes, supporting its use in mechanistic studies of synaptic signaling.
NR3A CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the GRIN3A gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the GRIN3A together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the GRIN3A open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish NR3A protein expression.
This CRISPR knockout system enables efficient generation of GRIN3A-deficient cell models for investigation of NR3A signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting GRIN3A exon(s) critical for NR3A function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple GRIN3A genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by NR3A CRISPR/Cas9 KO Plasmid (h) and NR3A CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the GRIN3A locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by NR3A HDR Plasmid (h) and NR3A HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by GRIN3A homology arms to support homology-directed repair at defined GRIN3A target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.