NR3B CRISPR/Cas9 KO Plasmid (h): sc-406162
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- NR3B 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 NR3B 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 | |
NR3B CRISPR/Cas9 KO Plasmid (h) | sc-406162 | 20 µg | $397.00 |
Overview
GRIN3B encodes the NR3B subunit of N-methyl-D-aspartate (NMDA) receptors, a class of ionotropic glutamate receptors that regulate excitatory synaptic transmission and Ca²⁺-dependent signaling in the central nervous system. Incorporation of NR3-family subunits can alter receptor biophysics, including agonist sensitivity and channel properties, thereby tuning synaptic plasticity and activity-dependent gene regulation. GRIN3B-linked modulation of glutamatergic signaling intersects with pathways controlling neuronal development, circuit refinement, and calcium homeostasis. Dysregulated NMDA receptor function is relevant to studies of neurodevelopmental and neuropsychiatric phenotypes, excitotoxic stress responses, and mechanisms of altered synaptic connectivity.
NR3B CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the GRIN3B gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the GRIN3B 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 GRIN3B 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 NR3B protein expression.
This CRISPR knockout system enables efficient generation of GRIN3B-deficient cell models for investigation of NR3B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting GRIN3B exon(s) critical for NR3B 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 GRIN3B genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by NR3B CRISPR/Cas9 KO Plasmid (h) and NR3B CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the GRIN3B locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by NR3B HDR Plasmid (h) and NR3B HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by GRIN3B homology arms to support homology-directed repair at defined GRIN3B 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.