NMDAε1 CRISPR/Cas9 KO Plasmid (h): sc-400963
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NMDAε1 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 NMDAε1 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
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: NMDAε1 Antibody (E-4): sc-515148
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NMDAε1 CRISPR/Cas9 KO Plasmid (h) | sc-400963 | 20 µg | $397.00 |
Overview
GRIN2A encodes the NMDA receptor subunit NMDAε1 (GluN2A), a glutamate-gated ion channel component that assembles with other NMDA receptor subunits to mediate Ca²⁺-permeable excitatory neurotransmission. This subunit helps define receptor kinetics and synaptic signaling strength, supporting activity-dependent synaptic plasticity processes such as long-term potentiation and long-term depression. NMDAε1 participates in postsynaptic signaling networks that couple ion flux to CaMK/CREB-dependent transcriptional programs and broader excitatory/inhibitory circuit homeostasis. Genetic variation or dysregulation of GRIN2A has been associated with neurodevelopmental and epilepsy-spectrum phenotypes and has been studied in the context of synaptic dysfunction relevant to neurological disease mechanisms.
NMDAε1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the GRIN2A gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the GRIN2A 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 GRIN2A 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 NMDAε1 protein expression.
This CRISPR knockout system enables efficient generation of GRIN2A-deficient cell models for investigation of NMDAε1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting GRIN2A exon(s) critical for NMDAε1 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 GRIN2A genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by NMDAε1 CRISPR/Cas9 KO Plasmid (h) and NMDAε1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the GRIN2A locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by NMDAε1 HDR Plasmid (h) and NMDAε1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by GRIN2A homology arms to support homology-directed repair at defined GRIN2A 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.