NMDAε4 CRISPR/Cas9 KO Plasmid (m): sc-420692
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NMDAε4 CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 NMDAε4 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: NMDAε4 Antibody (G-10): sc-17822
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
NMDAε4 CRISPR/Cas9 KO Plasmid (m) | sc-420692 | 20 µg | $397.00 |
Overview
Grin2d encodes the mouse NMDA receptor subunit NMDAε4 (GluN2D), a glutamate-gated ion channel component that shapes excitatory synaptic transmission through voltage- and ligand-dependent Ca²⁺ influx. Incorporation of NMDAε4 influences receptor kinetics and Mg²⁺ sensitivity, thereby modulating synaptic plasticity, activity-dependent gene expression, and neuronal network development. NMDA receptor signaling interfaces with CaMK/CREB and other calcium-dependent pathways that couple synaptic activity to transcriptional programs and circuit maturation. Altered NMDAε4 function or subunit composition is frequently studied in the context of neurodevelopmental and neuropsychiatric phenotypes, as well as seizure susceptibility and excitotoxic stress paradigms.
NMDAε4 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Grin2d gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Grin2d 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 Grin2d 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 NMDAε4 protein expression.
This CRISPR knockout system enables efficient generation of Grin2d-deficient cell models for investigation of NMDAε4 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Grin2d exon(s) critical for NMDAε4 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 Grin2d genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by NMDAε4 CRISPR/Cas9 KO Plasmid (m) and NMDAε4 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Grin2d locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by NMDAε4 HDR Plasmid (m) and NMDAε4 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Grin2d homology arms to support homology-directed repair at defined Grin2d 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.